Cardiovascular diseases modified
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  • 1. CARDIOVASCULAR DISEASES
    Nelia B. Perez RN, MSN
    PCU – MJCN
    BSN 2013
  • 2. THE CARDIOVASCULAR SYSTEM
  • 3. GENERAL CARDIAC ASSESSMENT
    Health history
    Demographic information
    Family/genetic history
    Cultural/social factors
    Risk factors
    Modifiable: High blood cholesterol, obesity, smoking, stress, hypertension, diabetes mellitus.
    Nonmodifiable: Family history, increasing age, gender, race
  • 4. Pathophysiology
  • 5.
  • 6. ASSESSING CHEST PAIN
  • 7. COMPARISON OF PHYSICAL CAUSES OF CHEST PAIN
  • 8. COMPARISON OF PHYSICAL CAUSES OF CHEST PAIN
  • 9. Angina Pectoris / Myocardial Ischemia
    • Ischemia – suppressed blood flow
    • 10. Angina – to choke
    • 11. Occurs when blood supply is inadequate to meet the heart’s metabolic demands
    • 12. Symptomatic paroxysmal chest pain or pressure sensation associated with transient ischemia
  • Pathophysiology
  • 13. Types
    Stable angina – the common initial manifestation of a heart disease
    • Common cause: atherosclerosis (although those with advance atherosclerosis do not develop angina)
    • 14. Pain is precipitated by increased work demands of the heart (i.e.. physical exertion, exposure to cold, & emotional stress)
    • 15. Pain location: precordial or substernal chest area
    • Pain characteristics:
    • 16. constricting, squeezing, or suffocating sensation
    • 17. Usually steady, increasing in intensity only at the onset & end of attack
    • 18. May radiate to left shoulder, arm, jaw, or other chest areas
    • 19. Duration: < 15mins
    • 20. Relieved by rest (preferably sitting or standing with support) or by use of NTG
  • Variant/Vasospastic Angina (Prinzmetal Angina)
    • 1st described by Prinzmetal & Associates in 1659
    • 21. Cause: spasm of coronary arteries (vasospasm) due to coronary artery stenosis
    • 22. Mechanism is uncertain (may be from hyperactive sympathetic responses, mishandling defects of calcium in smooth vascular muscles, reduced prostaglandin I2 production)
    • Pain Characteristics: occurs during rest or with minimal exercise
    - commonly follows a cyclic or regular pattern of occurrence (i.e.. Same time each day usually at early hours)
    • If client is for cardiac cath, Ergonovine (nonspecific vasoconstrictor) may be administered to evoke anginal attack & demonstrate the presence & location of spasm
  • Cont…
    Nocturnal Angina - frequently occurs nocturnally (may be associated with REM stage of sleep)
    Angina Decubitus – paroxysmal chest pain occurs when client sits or stands up
    Post-infarction Angina – occurs after MI when residual ischemia may cause episodes of angina
  • 23. Cont…
    • Dx: detailed pain history, ECG, TST, angiogram may be used to confirm & describe type of angina
    • 24. Tx: directed towards MI prevention
    • 25. Lifestyle modification (individualized regular exercise program, smoking cessation)
    • 26. Stress reduction
    • 27. Diet changes
    • 28. Avoidance of cold
    • 29. PTCA (percutaneoustransluminal coronary angioplasty) may be indicated if with severe artery occlusion
  • Drug Therapy
    • Nitroglycerin (NTGs) – vasodilators:
    • 30. patch (Deponit, Transderm-NTG)
    • 31. sublingual (Nitrostat)
    • 32. oral (Nitroglyn)
    • 33. IV (Nitro-Bid)
    • 34. Β-adrenergic blockers:
    • 35. Propanolol (Inderal)
    • 36. Atenolol (Tenormin)
    • 37. Metoprolol (Lopressor)
    • 38. Calcium channel blockers:
    • 39. Nifedipine (Calcibloc, Adalat)
    • 40. Diltiazem (Cardizem)
    • 41. Lipid lowering agents –statins:
    • 42. Simvastatin
    • 43. Anti-coagulants:
    • 44. ASA (Aspirin)
    • 45. Heparin sodium
    • 46. Warfarin (Coumadin)
  • Classification
    • Class I – angina occurs with strenuous, rapid, or prolonged exertion at work or recreation
    • 47. Class II – angina occurs on walking or going up the stairs rapidly or after meals, walking uphill, walking more than 2 blocks on the level or going more than 1 flight of ordinary stairs at normal pace, under emotional stress, or in cold
    • 48. Class III – angina occurs on walking 1-2 blocks on the level or going 1 flight of ordinary stairs at normal pace
    • 49. Class IV – angina occurs even at rest
  • Nursing Management
    • Diet instructions (low salt, low fat, low cholesterol, high fiber); avoid animal fats
    • 50. E.g.. White meat – chicken w/o skin, fish
    • 51. Stop smoking & avoid alcohol
    • 52. Activity restrictions are placed within client’s limitations
    • 53. NTGs – max of 3doses at 5-min intervals
    • 54. Stinging sensation under the tongue for SL is normal
    • 55. Advise clients to always carry 3 tablets
    • 56. Store meds in cool, dry place, air-tight amber bottles & change stocks every 6months
    • 57. Inform clients that headache, dizziness, flushed face are common side effects.
  • Nursing Management
    • Do not discontinue the drug.
    • 58. For patches, rotate skin sites usually on chest wall
    • 59. Instrct on evaluation of effectiveness based on pain relief
    • 60. Propanolols causes bronchospasm & hypoglycemia, do not administer to asthmatic & diabetic clients
    • 61. Heparin – monitor bleeding tendencies (avoid punctures, use of soft-bristled toothbrush); monitor PTT levels; usedfor 2wks max; do not massage if via SC; have protaminesulfate available
    • 62. Coumadin – monitor for bleeding & PT; always have vit K readily available (avoid green leafyveggies)
  • Acute Coronary Syndrome
    • Unstable Angina/Non ST-Segment Elevation MI – a clinicalsyndrome of myocardial ischemia
    • 63. Causes: atherosclerotic plaque disruption or significant CHD, cocaine use (risk factor)
    • 64. Defining guidelines: (3 presentations)
    Symptoms at rest (usually prolonged, i.e.. >20mins)
    New onset exertional angina (increased in severity of at least 1 class – to at least class III) in <2months
    Recent acceleration of angina to at least class III in <2months
  • 65.
    • Dx: based on pain severity & presenting symptoms, ECG findings & serum cardiac markers
    • 66. When chest pain has been unremitting for >20mins, possibility of ST-Segment Elevation MI is usually considered
  • Cont…
    • ST-Segment Elevation MI (Heart Attack)
    • 67. Characterized by ischemic death of myocardial tissue associated with atherosclerotic disease of coronary arteries
    • 68. Area of infarction is determined by the affected coronary artery & its distribution of blood flow (right coronary artery, left anterior descending artery, left circumflex artery)
    • Dx: based on presenting S/Sx, serum markers, & ECG (changes may not be present immediately after symptoms except dysrhythmias; PVCs/premature ventricular contractions are common after MI)
    • 69. Typical ECG changes: ST-segment elevation, Q wave prolongation, T wave inversion
  • Cont…(MI)
    Manifestations:
    • chest pain – severe crushing, constricting, “someone sitting on my chest”
    - substernal radiating to left arm, neck or jaw
    - prolonged (>35mins) & not relieved by rest
    • Shortness of breath, profuse perspiration
    • 70. Feeling of impending doom
    • Complications: death (usually within 1 hr of onset)
    • 71. Heart failure & cardiogenic shock – profound LV failure from massive MI resulting to low cardiac output
    • 72. Thromboemboli – leads to immobility & impaired cardiac function contributing to blood stasis in veins
    • 73. Rupture of myocardium
    • 74. Ventricular aneurysms – decreases pumping efficiency of heart & increases work of LV
  • Pathophysiology
    Causes: atherosclerotic heart disease,
    thrombosis/embolism,
    shock &/or hemorrhage, direct trauma
    Myocardial ischemia
    ↑cellular
    hypoxia
    ↓myocardial
    O2 supply
    ↓ myocardial contractility
    ↓cardiac output
    ↓arterial pressure
    Stimulation of sympathetic receptors
    ↑myocardial
    O2 demand
    ↑peripheral
    vasoconstriction
    ↑ afterload
    ↑ HR
    ↓myocardial
    tissue perfusion
    ↑diastolic
    filling
    ↑ myocardial
    contractility
  • 75. Tissue Changes After MI
  • 76. Management of MI
    • Initial Management: OMEN
    - O2 therapy via nasal prongs
    - adequate analgesia (Morphine via IV – also has vasodilator property)
    - ECG monitoring
    -sublingual NTG (unless contraindicated; IV may be given to limit infarction size & most effective if given within 4hrs of onset)
    • Thrombolytic Therapy – best results occur if initiated within 60-90mins of onset (Streptokinase & Urokinase – promote conversion of plasminogen to plasmin)
    • 77. Anti-arrhythmics: lidocaine, atropine, propanolol
    • 78. Anticoagulants & antiplatelets: ASA, heparin
    • 79. Stool softeners
  • Surgery :
    Revascularization
    PTCA
    Coronary stent implantation
    Coronary Artery Bypass Graft (CABG) – no response to medical treatment & PTCA
    Resection – aneurysm
  • 80.
  • 81. ASSESSMENT
    Subjective data:
    PAIN!!!
    Nausea
    SOB
    Apprehension
    Objective data:
    VS
    Diaphoresis
    Emotional restlessness
  • 82. ANALYSIS / NURSING DIAGNOSES
    Decreased cardiac output related to myocardial damage
    Impaired gas exchange related to poor perfusion, shock
    Pain related to myocardial ischemia
    Activity intolerance related to pain or inadequate oxygenation
    Fear related to possibility of death
  • 83. NURSING CARE PLAN
    Goal # 1: reduce pain / discomfort
    Narcotics – morphine; note response; Avoid IM
    Humidified oxygen 2-4 L/min; mouth care – O2 is drying
    Position: semi-Fowler’s to improve ventilation
  • 84. NURSING CARE PLAN
    Goal # 2: maintain adequate circulation; stabilize heart rhythm
    Monitor VS/UO; observe for cardiogenic shock
    Monitor ECG for arrhythmias
    Medications: antiarrhythmics; anticoagulants; thrombolytics
    Diagnostics: cardiac catheterizations, CAB surgery
    Recognize heart failure: edema, cyanosis, dyspnea, crackles
    Check labs: troponin, blood gases, electrolytes, clotting time
    CVP: (5-15 cm H2O) increases with heart failure
    ROM of lower extremities; antiembolic stockings
  • 85. NURSING CARE PLAN
    Goal # 3: decrease oxygen demand/promote oxygenation, reduce cardiac workload
    O2 as ordered
    Activity: bedrest (24-48 H) with bedside commode; planned rest periods; control visitors
    Position: semi-Fowler’s to facilitate lung expansion and decrease venous return
    Anticipate needs of client: call light, water / Reassurance
    Assist with feeding, turning
    Environment: quiet and comfortable
    Medications: CCBs, vasodilators, cardiotonics
  • 86. NURSING CARE PLAN
    Goal # 4: maintain fluid electrolyte, nutritional status
    IV (KVO); CVP; vital signs
    UO: 30 cc/hr
    Labs: electrolytes (Na, K, Mg)
    Monitor ECG
    Diet: progressive low calorie, low sodium, low cholesterol, low fat, without caffeine
  • 87. NURSING CARE PLAN
    Goal # 5: facilitate fecal elimination
    Medications: stool softeners to prevent Valsalva maneuver; mouth breathing during bowel movement
    Bedside commode
  • 88. NURSING CARE PLAN
    Goal # 6: provide emotional support
    Recognize fear of dying: denial, anger, withdrawal
    Encourage expression of feelings, fears, concerns
    Discuss rehabilitation, lifestyle changes: prevent cardiac-invalid syndrome by promoting self-care activities, independence
  • 89. NURSING CARE PLAN
    Goal # 7: promote sexual functioning
    Encourage verbalization of concerns regarding activity, inadequacy, limitations, expectations – include partner (usually resume activity 5-8 wks after uncomplicated MI or when client can climb 2 flights of stairs
    Identify need for referral for sexual counselling
  • 90. NURSING CARE PLAN
    Goal # 8: health teaching
    Diagnosis and treatment regimen
    Caution when to avoid sexual activity: after heavy meal, alcohol ingestion; when fatigued, stressed; with unfamiliar partners; in extreme temperatures
    Information about sexual activity: less fatiguing positions
    Support groups / Follow-up care
    Medications: administration, importance, untoward effects; pulse taking
    Control risk factors: rest, diet, exercise, no smoking, weight control, stress reduction
  • 91. EVALUATION
    No complications: stable vital signs; relief of pain
    Adheres to medication regimen
    Activity tolerance is increased
    Reduction or modification of risk factors
  • 92. CONGESTIVE HEART FAILURE
    inability of the heart to pump sufficient blood to meet the needs of the tissue for oxygen and nutrient.
  • 93. PATHOPHYSIOLOGY
  • 94. ASSESSMENT
    Subjective data:
    Shortness of breath
    Orthopnea (sleeps on two or more pillows)
    Paroxysmal nocturnal dyspnea (sudden breathlessness during sleep)
    Dyspnea on exertion (climbing stairs)
    Apprehension; anxiety; irritability
    Fatigue; weakness
    Reported weight gain; feeling of puffiness
  • 95. ASSESSMENT
    Objective data:
    VS:
    BP: decreasing systolic; narrowing pulse pressure
    Pulse: pulsusalternans (alternating strong-weak-strong cardiac contraction); increased.
    Respirations: crackles; Cheyne-Stokes
    Edema: dependent, pitting (1+ to 4+ mm)
    Liver: enlarged, tender
    Distended neck veins
    Chest X-ray: enlarged heart; dilated pulmonary vessels; lung edema
  • 96. Left Ventricular Compared with Right Ventricular Heart Failure
  • 97. ANALYSIS / NURSING DIAGNOSES
    Decreased cardiac output related to decreased myocardial contractility
    Activity intolerance related to generalized body weakness and inadequate oxygenation
    Fatigue related to edema and poor oxygenation
  • 98. Fluid volume excess related to compensatory mechanisms
    Impaired gas exchange related to pulmonary congestion
    Anxiety related to shortness of breath
    Sleep pattern disturbance related to paroxysmal nocturnal disturbance
  • 99. NURSING CARE PLAN
    Goal # 1: provide physical rest/ reduce emotional stimuli
    Position: sitting or semi-Fowler’s until tachycardia, dyspnea, edema resolved; change position frequently; pillows for support
    Rest: planned periods; limit visitors, activity, noise. Chair and commode privileges
    Support: stay with client who is anxious; have family member who is supportive present; administer sedatives/tranquilizers as ordered
    Warm fluids if appropriate
  • 100. NURSING CARE PLAN
    Goal # 2: provide for relief of respiratory distress; reduce cardiac workload
    Oxygen: low flow rate; encourage deep breathing (5-10 min q 2H); auscultate breath sounds for congestion, pulmonary edema.
    Position: elevating head of bed 20-25 cm (8-10 in) alleviates pulmonary congestion
    Medications – digitalis, ACE inhibitors, inotropic agents, diuretics, tranquilizers, vasodilators
  • 101. NURSING CARE PLAN
    Goal # 3: provide for special safety needs
    Skin care:
    Inspect, massage, lubricate bony prominences
    Use foot cradle, heel protectors; sheepskin
    Side rails up if hypoxic (disoriented)
    Vital signs: monitor for signs of fatigue, pulmonary emboli
    ROM: active, passive; elastic stockings
  • 102. NURSING CARE PLAN
    Goal # 4: maintain fluid and electrolyte balance, nutritional status
    Urine output: 30 cc/hr minimum; estimate insensible loss in client who s diaphoretic. Monitor BUN, serum creatinine, and electrolytes.
    Daily weight; same time, clothes, scale
    IV: IV infusion pump to avoid circulatory overload; strict I/O
    Diet
    Low sodium
    Small, frequent feedings
    Discuss food preferences with client.
  • 103. NURSING CARE PLAN
    Goal # 5: health teaching
    Diet restrictions; meal preparation
    Activity restrictions; planned rest periods
    Medications: schedule (e.g. diuretics in early morning); purpose; dosage; side effects (pulse taking, daily weights, intake of potassium-containing foods)
    Refer to available communityresources for dietary assistance, weight reduction, exercise program.
  • 104. EVALUATION
    Increase in activity level tolerance – fatigue decreased
    No complications – pulmonary edema, respiratory distress
    Reduction in dependent edema
  • 105. DAY 3
    of
    Cardiovascular
    diseases
  • 106. hyperlipidemia means high lipid levels. 
    High lipid levels can speed up a process called atherosclerosis, or hardening of the arteries.
  • 107. Most hyperlipidemia is caused by lifestyle habits or treatable medical conditions. Lifestyle contributors include obesity, not exercising, and smoking. Conditions that cause hyperlipidemia include diabetes, kidney disease, pregnancy, and an underactive thyroid gland.
  • 108. You can also inherit hyperlipidemia. The cause may be genetic if you have a normal body weight and other members of your family have hyperlipidemia.
  • 109. You have a greater chance of developing hyperlipidemia if you are a man older than age 45 or a woman older than age 55. If a close relative had early heart disease (father or brother affected before age 55, mother or sister affected before age 65), you also have an increased risk.
  • 110. Treatment of Hyperlipidemia
    It is necessary to first identify and treat any potential underlying medical problems, such as diabetes or hypothyroidism, that may contribute to hyperlipidemia. Treatment of hyperlipidemia itself includes dietary changes, weight reduction and exercise. If lifestyle modifications cannot bring about optimal lipid levels, then medications may be necessary.
  • 111. Medications most commonly used to treat high LDL cholesterol levels are statins, such as atorvastatin (Lipitor) or simvastatin (Mevacor). These medications work by reducing the production of cholesterol within the body. 
  • 112. CARDIOMYOPATHIESHeart muscle disease associated with cardiac dysfunction
    CARDIOMYOPATHIES
    1. Dilated Cardiomyopathy
    2. Hypertrophic Cardiomyopathy
    3. Restrictive cardiomyopathy
  • 113. DILATED CARDIOMYOPATHY ASSOCIATED FACTORS
    1. Heavy alcohol intake
    2. Pregnancy
    3. Viral infection
    4. Idiopathic
  • 114. DILATED CARDIOMYOPATHYPATHOPHYSIOLOGY
    Diminished contractile proteins - poor contraction -decreased blood ejection -increased blood remaining in the ventricle -ventricular stretching and dilatation.-
    SYSTOLIC DYSFUNCTION
  • 115. HYPERTROPHIC CARDIOMYOPATHY
    Associated factors:
    1. Genetic
    2. Idiopathic
  • 116. HYPERTROPHIC CARDIOMYOPATHY
    Pathophysiology
    Increased size of myocardium - reduced ventricular volume - increased resistance to ventricular filling - diastolic dysfunction
  • 117. RESTRICTIVE CARDIOMYOPATHY
    Associated factors
    1. Infiltrative diseases like AMYLOIDOSIS
    2. Idiopathic
  • 118. RESTRICTIVE CARDIOMYOPATHYPathophysiology
    Rigid ventricular wall -impaired stretch and diastolic filling -decreased output - Diastolic dysfunction
  • 119. CARDIOMYOPATHIES
    Assessment findings
    1. PND
    2. Orthopnea
    3. Edema
    4. Chest pain
    5. Palpitations
    6. dizziness
    7. Syncope with exertion
  • 120. CARDIOMYOPATHIES
    Laboratory Findings
    1. CXR- may reveal cardiomegaly
    2. ECHOCARDIOGRAM
    3. ECG
    4. Myocardial Biopsy
  • 121. CARDIOMYOPATHIES
    Medical Management
    1. Surgery
    2. pacemaker insertion
    3. Pharmacological drugs for symptom relief
  • 122. CARDIOMYOPATHIES
    Nursing Management
    1.Improve cardiac output
    Adequate rest
    Oxygen therapy
    Low sodium diet
  • 123. CARDIOMYOPATHIES
    Nursing Management
    2. Increase patient tolerance
    Schedule activities with rest periods in between
  • 124. CARDIOMYOPATHIES
    Nursing Management
    3. Reduce patient anxiety
    Support
    Offer information about transplantations
    Support family in anticipatory grieving
  • 125. Infective endocarditis
    Infection of the heart valves and the endothelial surface of the heart
    Can be acute or chronic
  • 126. Infective endocarditis
    Etiologic factors
    1. Bacteria- Organism depends on several factors
    2. Fungi
  • 127. Infective endocarditis
    Risk factors
    1. Prosthetic valves
    2. Congenital malformation
    3. Cardiomyopathy
    4. IV drug users
    5. Valvular dysfunctions
  • 128. 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
  • 129. Infective endocarditis
    Assessment findings
    1. Intermittent HIGH fever
    2. anorexia, weight loss
    3. cough, back pain and joint pain
    4. splinter hemorrhages under nails
  • 130. Infective endocarditis
    Assessment findings
    5. Osler’s nodes- painful nodules on fingerpads
    6. Roth’s spots- pale hemorrhages in the retina
  • 131. Infective endocarditis
    Assessment findings
    7. Heart murmurs
    8. Heart failure
  • 132. Infective endocarditis
    Prevention
    Antibiotic prophylaxis if patient is undergoing procedures like dental extractions, bronchoscopy, surgery, etc.
  • 133. Infective endocarditis
    LABORATORY EXAM
    Blood Cultures to determine the exact organism
  • 134. Infective endocarditis
    Nursing management
    1. regular monitoring of temperature, heart sounds
    2. manage infection
    3. long-term antibiotic therapy
  • 135. Infective endocarditis
    Medical management
    1. Pharmacotherapy
    IV antibiotic for 2-6 weeks
    Antifungal agents are given – amphotericin B
  • 136. Infective endocarditis
    • Medical management
    • 137. 2. Surgery
    • 138. Valvular replacement
  • CARDIOGENIC SHOCK
    • Heartfailsto pump adequately resulting to a decreased cardiac output and decreased tissue perfusion
    • 139. ETIOLOGY
    • 140. 1. Massive MI
    • 141. 2. Severe CHF
    • 142. 3. Cardiomyopathy
    • 143. 4. Cardiac trauma
    • 144. 5. Cardiac tamponade
  • 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
  • 145. CARDIOGENIC SHOCK
    LABORATORY FINDINGSIncreased CVP
    Normal is 4-10 cmH2O
  • 146. CARDIOGENIC SHOCK
    • NURSING INTERVENTIONS
    • 147. 1. Place patient in a modified Trendelenburg (shock ) position
    • 148. 2. Administer IVF, vasopressors and inotropics such as DOPAMINE and DOBUTAMINE
    • 149. 3. Administer O2
    • 150. 4. Morphine is administered to decreased pulmonary congestion and to relieve pain
  • CARDIOGENIC SHOCK
    • 5. Assist in intubation, mechanical ventilation, PTCA, CABG, insertion of Swan-Ganzcath and IABP
    • 151. 6. Monitor urinary output, BP and pulses
    • 152. 7. cautiously administer diuretics and nitrates
  • CARDIAC TAMPONADE
    A condition where the heart is unable to pump blood due to accumulation of fluid in the pericardial sac (pericardial effusion)
  • 153. CARDIAC TAMPONADE
    • This condition restricts ventricular filling resulting to decreased cardiac output
    • 154. Acute tamponade may happen when there is a sudden accumulation of more than 50 ml fluid in the pericardial sac
  • CARDIAC TAMPONADE
    • Causative factors
    • 155. 1. Cardiac trauma
    • 156. 2. Complication of Myocardial infarction
    • 157. 3. Pericarditis
    • 158. 4. Cancer metastasis
  • CARDIAC TAMPONADE
    • ASSESSMENT FINDINGS
    • 159. 1. BECK’s Triad- Jugular vein distention, hypotension and distant/muffled heart sound
    • 160. 2. Pulsusparadoxus
    • 161. 3. Increased CVP
    • 162. 4. decreased cardiac output
  • CARDIAC TAMPONADE
    • ASSESSMENT FINDINGS
    • 163. 5. Syncope
    • 164. 6. anxiety
    • 165. 7. dyspnea
    • 166. 8. Percussion- Flatness across the anterior chest
  • CARDIAC TAMPONADE
    • Laboratory FINDINGS
    • 167. 1. Echocardiogram
    • 168. 2. Chest X-ray
  • CARDIAC TAMPONADE
    • NURSING INTERVENTIONS
    • 169. 1. Assist in PERICARDIOCENTESIS
    • 170. 2. Administer IVF
    • 171. 3. Monitor ECG, urine output and BP
    • 172. 4. Monitor for recurrence of tamponade
    • Pericardiocentesis
    • 173. Patient is monitored by ECG
    • 174. Maintain emergency equipments
    • 175. Elevate head of bed 45-60 degrees
    • 176. Monitor for complications- coronary artery rupture, dysrhythmias, pleural laceration and myocardial trauma
  • HYPERTENSION
    A systolic BP greater than 140 mmHg and a diastolic pressure greater than 90 mmHg over a sustained period, based on two or more BP measurements .
  • 177. HYPERTENSION
    • Types of Hypertension
    • 178. 1. Primary or ESSENTIAL
    • 179. Most common type
    • 180. 2. Secondary
    • 181. Due to other conditions like Pheochromocytoma, renovascular hypertension, Cushing’s, Conn’s , SIADH
  • 182.
  • 183.
  • 184. Alterations inBlood Flow in the Systemic Circulation
  • 185. Buerger’s Disease
    Also known as Thromboangiitisobliterans
    Usually a disease of heavy cigarette smoker/tobacco user men, 25-40y/o
    Inflammatory arterial disorder that causes thrombus formation often extends to adjacent veins & nerves
  • 186. Affects medium-sized arteries (usually plantar & digital vessels in the foot or lower legs)
    unknown pathogenesis but it had been suggested that:
    tobacco may trigger an immune response or
    unmask a clotting defect;
    -> these 2 can incite an inflammatory reaction of the vessel wall
  • 187. Manifestations
    • Pain – predominant symptom; R/T distal arterial ischemia
    • 188. Intermittent claudication in the arch of foot & digits
    • 189. Increased sensitivity to cold (due to impaired circulation
    • 190. Absent/diminished peripheral pulses
    • Color changes in extremity (cyanotic on dependent position; digits may turn reddish blue)
    • 191. Thick malformed nails (chronic ischemia)
    • 192. Disease progression ulcerate tissues & gangrenous changes may arise; may necessitate amputation
  • Diagnosis & Treatment
    Diagnostic methods – those that assess blood flow (Doppler ultrasound & MRI)
    Tx: mandatory to stop smoking or using tobacco
    Meds to increase blood flow to extremities
    Surgery (surgical sympathectomy)
    amputation
  • 193. Rynaud’s Disease
    • Mechanism: intensive vasospasm of arteries & arterioles in thefingers
    • 194. Cause: unknown
    • 195. Usually affects young women
    • 196. Precipitated by exposure to cold & strong emotions
    • 197. Raynaud’s phenomenon – associated with previous injury (i.e.. Frostbite, occupational trauma associated with use of heavy vibrating tools, collagen diseases, neuro d/o, chronic arterial occlusive d/o)
  • Manifestations
    Period of ischemia (ischemia due to vasospasm)
    change in skin color = pallor to cyanotic
    1st noticed at the fingertips later moving to distal phalanges
    Cold sensation
    Sensory perception changes (numbness & tingling)
    Period of hyperemia – intense redness
    Throbbing
    Paresthesia
  • 198. Return to normal color
    Note: although all of the fingers are affected symmetrically, only 1-2digits may be involved
    Severe cases: arthritis may arise (due to nutritional impairment)
    Brittle nails
    Thickening of the skin of fingertips
    Ulceration & superficial gangrene of fingers (rare occasions)
  • 199. Diagnosis & Treatment
    • Dx: initial = based on Hx of vasospastic attacks
    • 200. Immersion of hand in cold water to initiate attack aids in the Dx
    • 201. Doppler flow velocimetry – used to quantify blood flow during temperature changes
    • 202. Serial Computed thermography (finger skin temp) – for diagnosing the extent of disease
    • Tx: directed towards eliminating factors causing vasospasm & protecting fingers from injury during ischemic attacks
    • 203. PRIORITIES: Abstinence in smoking & protection from cold
    • 204. Avoidance of emotional stress (anxiety & stress may precipitate vascular spasm)
    • 205. Meds: avoid vasoconstrictors (i.e.. Decongestants)
    -Calcium channel blockers (Diltiazem, Nifedipine, Nicardipine) – decrease episodes of attacks
  • 206. Care Plan for Clients with Altered Cardiovascular Oxygenation
    Goals:
    Relief of pain & symptoms
    Prevention of further cardiac damage
    Nursing Interventions:
    Pain control
    Proper medications
    Decrease client’s anxiety
    Health teachings (meds, activities, diet, exercise, etc)
    Assessment:
    Hx of symptoms (pain, esp. chest pain; palpitations; dyspnea)
    v/s
    Nursing Dx:
    ineffective tissue perfusion (cardiopulmonary)
    Impaired gas exchange
    Anxiety due to fear of death (clients with MI or Angina)