patho 4 CV - Vickers

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  1. How does the blood flow through the heart?
    oxygenated blood enters left atrium through the aortic valve -> through mitral/bicuspid valve ->left ventricle -> pumps blood out the aorta -> arteries -> arterioles -> capillaries -> venules -> veins -> vena cava -> deox blood enters right atrium -> thru tricuspid valve -> right ventricle -> thru the pulmonary valve -> pulmonary artery -> lungs to be oxygenated -> pulmonary veins -> oxygenated blood reenters left atrium
  2. Function of arterial blood flow?
    take blood away from the heart to tissues
  3. Function of venous blood flow?
    collects blood from body tissues and takes it back to the R side of the heart where it is pumped to the lungs for reoxygenation
  4. Conduction system of the heart?
    SA node -> AV node -> bundle branches -> Purkinje fibers
  5. What occurs during systole and diastole of the cardiac cycle?
    during diastole the ventricles relax and the mitral and tricuspid valves open to allow blood to enter the ventricles passively from the atria; at the end of diastole the atria contract and propel remaining blood into ventricles & AV valves shut to prevent backflow into atria

    during systole the ventricles contract and the pulmonary and aortic valves open to allow blood to flow out of the heart to the tissues and lungs; the AV valves are closed to prevent blood flowing back into the atria
  6. 2 valves on the left side of the body?
    mitral and aortic
  7. 2 valves on right side of the heart?
    tricuspid and pulmonic
  8. What is result of clots in the venous system?
    pulmonary embolism
  9. Result of clot in the artery of a leg?
    will clog in foot and cause ischemia
  10. Is artery or vein more critical if a clot occurs?
    artery b/c it causes ischemia of a body part
  11. Firing mechanism in the heart?
    SA node
  12. Normal CO?
    8 liters per minute
  13. CO = ?
    SV X HR

    won't have to figure that on the test
  14. How do you know if pt has good cardiac output?
    pulse, BP, appearance, color, skin moisture,
  15. If bad CO what is the appearance?
    pale and diaphoretic, v/s, mottled (white/yellow/purple due to ischemia of tissues), grey, capillary refill, MM
  16. Preload?
    amount of blood the heart must pump with each beat due to amnt of blood coming from veins
  17. Afterload?
    how much pressure that is required for the heart to pump blood out
  18. CHF CO?

    Goal of TX?

    HOw is this done?
    decreased CO

    increase CO without increases the workload of the heart

    drugs that affect preload and afterload
  19. CO?
    amount of blood the heart pumps in a minute
  20. What happens in preload is increased?

    How can preload be decreased?
    will increase CO

    1. sit pt on side of the bed and let legs hang off so blood volume stays in the legs

    2. give them diuretics to decrease BV

    3. give them drugs that vasodilate - will decrease volume coming to heart
  21. Vasodilator effects?
    will keep blood volume in legs and decrease preload
  22. ACE inhibitors?
    vasodilators - decrease preload
  23. Vasoconstriction effects on afterload?
    increases it b/c small vessels increase pressure needed to get blood through
  24. High blood pressure effects on heart?
    causes blood vessels to be constricted that more volume comes to heart and afterload is increased - heart is overworked
  25. Compensatory mechanisms of the body effect?

    What are interventions for?
    they make prob worse

    interventions are all to counteract compensatory mechanisms of the body
  26. 3 goals of cardiac treatment?
    increase CO, decrease preload & afterload
  27. Cardiac contractility?
    ability of the heart to change its force of contractions
  28. Drug that can increase cardiac contractility?
    digoxin, lanoxin
  29. MAP?


    Normal MAP?
    mean arterial pressure

    • (2 X diastolic) + systolic
    •                 3

    must be at least 60
  30. Why does diastolic pressure count 2 X more in MAP?
    2/3 of the cardiac cycle is spent in diastole
  31. Increased HR effect on CO?
    can decrease CO
  32. Tissue factors that contribute to local control of blood flow?
    histamine, serotonin, kinins, prostaglandins, blood vessels, endothelial control of vasodilation and vasoconstriction, NO (nitrous oxide)
  33. Histamine affect on blood flow to an area?
    increases blood flow to area
  34. Serotonin effect on blood flow to an area?
    vasoconstriction = less blood flow to the area
  35. kinins effect on blood flow to an area?
    VASOCONSTRICTION = less blood flow to the area
  36. 2 prostaglandins and their effects on blood flow to an area?
    Prostaglandin E - vasodilator - increases

    Prostaglandin F - vasoconstrictor - decreases
  37. NO?

    Effect on blood flow to an area?
    nitrous oxide

    powerful vasodilator produced by the endothelial lining of arteries - increases blood flow to an area
  38. Collateral circulation AKA?
  39. Why would a 70 year old pt live from MI but a 40 year old die?
    70 year old has had ischemia a while and collateral circulation has had time to develop
  40. If a pt has good collateral circulation what would be the Tx?
    nitroglyceran to keep collateral circulation open and decrease chest pain
  41. Parasympathetic NS regulates HR through ____ nerve with increase vagal activity producing ______ HR.

  42. What is a way a nurse can nonmedically raise a pt HR?
    Have them "vagal down"  bear down like having a bowel movement
  43. SNS effect on the heart?
    excitatory influence on heart rate and contractility
  44. Teaching for a pt that does need their HR to go up?

    vagal can cause decrease BF to the brain and MI

    will give them stool softeners
  45. 2 ways that vagal can occur?
    bearing down in any way

    holding breath in anticipation of pain, etc
  46. Main carrier of cholesterol?
  47. 2 types of lipids that are primarily ass. with hyperlipidemia?
    1. cholesterol

    2. triglycerides
  48. Main S/S of venous problem in the legs?


    Diff in Tx of arterial prob in legs?
    swelling in the legs

    elevate legs

    in arterial will keep legs down to try to increase BF
  49. Arterial problems?
    hyperlipidemia, PAD, Raynaud disease, aneurysms,
  50. 2 sites of lipoprotein synthesis?
    small intestine and liver
  51. If a person has a blockage in their arteries what will it be caused by?
  52. HDL effect on cholesterol?
    lowers it by transporting it back to liver to be excreted
  53. 2 ways to increase HDL?
    moderate alcohol intake and exercise
  54. _____ decreases HDL/
  55. Primary hypercholesteremia?
    genetic basis - not necessarily r/t what they eat or the size of the person
  56. Secondary hypercholesterolemia?
    obesity and high calorie diets

  57. Drugs for hypercholesterolemia?
    statins that work on liver and have it decrease cholesterol production
  58. Dx and screening for hypercholesterolemia?
    all adults 20 yrs and older have a fasting lipoprotein profile done q 5 yrs
  59. Total cholesterol normal?

    HDL normal?
    < 200 mg/dL

    HDL > 40mg/dL
  60. Crestor?
    turns liver off at night
  61. Smoking effects on arteries?
    can damage the lining of the arteries, atherosclerosis will occur at the site of damage and arteries become more sticky due to smoking so the debris sticks to the artery more easily
  62. CHD?

    8 risk factors for CHD?
    coronary heart disease

    • 1. high LDL
    • 2. family Hx of premature CHD in 1st degree relative
    • 3. current cigarette smoking
    • 4. hypertension
    • 5. low HDL
    • 6. DM
    • 7. hypercholesterolemia
    • 8. male gender until women hit menopause
  63. Recommendations for total cholesterol in pt with no major risk factors, 2 or more risk factors, high risk factors, very high risk factors?
    no risk factors - 160mg/dL or less

    2 or more risk factors - <130 mg/dL

    high risk factors - (with CHD) - < 100 mg /dL

    very high risk factors (acute coronary syndromes) - < 70mg/dL
  64. Relationship of high risk factors for CHD and age?
    more risk factors = develop at earlier age
  65. Why are hypertension and smoking risk factors for CHD?
    they damage the arteries
  66. Why is DM a risk factor for CHD?
    sugar makes everything sticky and speeds atherosclerosis
  67. Pt teaching for pt that has started cholesterol meds?
    teach them they need to bake food and that they can't eat everything they want just because they have the med

    find out who is doing the cooking and teach them
  68. 3 types of atherosclerotic lesions?
    • 1. fatty streaks
    • 2. fibrous atheromatous
    • 3. complicated lesion
  69. Fatty streak lesions?
    present in CH but not sure they lead to atherosclerotic lesions
  70. Fibrous atheromatous lesions?
    clinical atherosclerosis

    lesion is a gray or pearly white elevated thickening of the vessel
  71. Complicated lesions characterized by ____, _______, _______,
    • 1. hemorrhage
    • 2. ulceration
    • 3. scar tissue deposits
  72. Most important complication of a complicated lesion?
    thrombosis caused by slow turbulent blood flow in the region of the plaque and ulceration of the plaque
  73. Most dangerous type of atherosclerotic lesion?

    complicated lesion b/c it can rupture and cause inflammatory process to occur which can lead to 100% occlusion
  74. Tx for thrombus from complicated lesion?
    anticoagulants, clot buster to disintergrate the clot and restore blood flow
  75. Modifiable risk factors for CHD?
    • 1. smoking cessation
    • 2. hypertension
    • 3. hyperlipidemia
    • 4. type II DM
  76. Unmodifiable risk factors for CHD?
    • 1. age
    • 2. gender
    • 3. genetic factors
    • 4. race
  77. Homocysteine effect on atherosclerosis?
    believed to increase risk for atherosclerosis by inhibiting anticoagulant cascade ass. and causing endothelial damage
  78. Protein that indicates systemic inflammation when elevated?

    May also indicate what?
    CRP - C-reactive protein

  79. What is the initiating factor in the dev of atherosclerosis?
    damage to endothelial vessel layer
  80. 4 EX factos that may damage the endothelial tissue layer and initiate atherosclerosis?
    • 1. smoking
    • 2. immune mechanisms
    • 3. mechanical stress - hypertension
    • 4. unstable plaques and complicated lesions
  81. Clinical manifestations of atherosclerosis?
    depends on vessel involved and how much narrowing there is

    ischemia V/S infarction - perfusion decrease v/s tissue death
  82. CHD?
    atherosclerosis of the coronary artery
  83. PAD? 

    Caused by?

    Who does it occur most in?
    peripheral artery disease -

    atherosclerosis / narrowed arteries reduce blood flow to the legs

    most common in 70-80 year old men
  84. 5 high risk factors for PAD?
    • 1. hypertension
    • 2. DM II
    • 3. hyperlipidemia
    • 4. cigarettes
    • 5. CHD / atherosclerosis in other areas
  85. Thromboangitis Obliterans?


    vasculitis of the med sized arteries of the hands and feet - become inflamed and swell - eventually block off the arteries and can cause ischemia of distal tissue

    AKA Buerger disease

    affects men b/t ages 25-40 who are heavy cig smokers
  86. Primary symptom of PAD?

    Why does this occur?
    intermittent claudication - pain with walking

    muscle is ischemic and requires more blood flow when being used - will do anaerobic respiration and cause lactic acid build up = pain in muscle

    at rest the pain goes away
  87. How to determine if a problem is arterial or venous when s/s is intermittent claudication:
    arterial: S/S of decreased blood flow/ischemia  thin/shiny skin, atrophy of leg muscle (chicken legs), cool extremity, popleteal and pedal pulses are weak or absent, hair loss on legs, elevation of leg causes color to blanch in leg, becomes deep red when leg is in dependent postion (dangling), brittle toenails,
  88. What should nurse do if can't find pedal pulse?
    dopplar the pulse and document it if found
  89. Positioning of legs for arterial blockage?
    not elevated
  90. Can you use heating pad for a pt with PAD?
    NO- they may have nerve damage due to decreased blood flow and may not be able to feel if it gets too hot

    can cause burns that will be hard to heal b/c of decreased BF
  91. Tx for PAD?
    • 1. walking (slowly) to the point of claudication usually is encouraged b/c it increases collateral circulation
    • 2. avoidance of injury
    • 3. no smoking
    • 4. Tx hypertension
    • 5. decrease lipids
    • 6. DM treatment
  92. Alcohol and bengay effect on PAD?
    will cause vasodilation and increase BF and decrease pain
  93. Thromboangitis Obliterans Tx?
    stop smoking
  94. Raynaud disease & phenomenon?
    functional disorder caused by intense vasospasm of arteries & arterioles in the fingers and less often in the toes
  95. Teaching pt with PAD?
    • 1. walk until it hurts and then rest and tell them why (increased collateral BF)
    • 2. need to avoid injury r/t decrease healing
    • 3. watch diet and weight if high cholesterol
    • 4. keep BG under control if DM
  96. Cause of thromboangitis obliterans?
    smoking - inflames vessels and cuts of blood flow to extremities = ischemia and amputation

    usually in fingers and toes then advances proximally and will have to keep getting amputations
  97. Who usually gets Raynaud disease?
    healthy young women
  98. Triggers of Raynaud's disease?
    • 1. smoking
    • 2. cold
    • 3. emotional stress
  99. Area usually affected by Raynauds disease?


    • 1. protect from cold
    • 2. decrease stressors/ triggers
    • 3. avoid injury r/t decreased BF
    • 4. no smoking
    • 5. Ca channel blockers
    • 6. Run hands under warm water
  100. 2 Meds that are give for Raynaud's disease?
    Ca channel blockers b/c treat spastic arteries

  101. Ca channel blockers effect on arteries?
    decreases spasms of arteries - given for spastic arteries
  102. Dx of Raynaud's disease?
    Hx of vasospastic attacks
  103. What happens when nitro and viagra are mixed?
    extremely low BP
  104. Complication with Raynaud's?
    if fingers are injured (paper cut) they will not heal well r/t decreased BF

    when BF is restored it hurts
  105. Aneurysm?
    weakened area of an artery causes small spherical dilation (outpouching) of the vessel at a bifurcation
  106. Where do aneurysms usually occur?

    What is a triple A?
    usually in aorta

    abdominal aortic aneurysm
  107. 2 ways aneurysms are usually found?
    • 1. umbilical pulsation - DO NOT PRESS ON IT
    • 2. Xray for other things - asymptomatic usually
  108. Typical triple A pt?
    man in their 70's b/c they have high blood pressure
  109. Hypertension effect on aneurysms?
    causes increased pressure and increased ballooning out of the aneurysms and possible rupture
  110. Who gets most triple A's?
    more in ppl over 50 and more in men
  111. 2 causes of triple A?
    • 1. atherosclerosis
    • 2. hypertension
  112. Where do most triple A's occur?
    elow the level of the renal artery and involve the bifurcation of the aorta and proximal end of the common iliac arteries
  113. Blood flow in an aneurysm?
    in the middle the blood is moving quickly and around the edges the blood is pooling

    • after Tx procedures must watch for clots
    • ---monitor I&O for renal clot
    • ---monitor perfusion
  114. Tx of aneurysms?
    • 1. < 5cm will just watch it
    • 2. > 5cm will go to surgery
    • 3. go to surgery if it is getting larger also
    • 4. interventional radiography - put in a graft to stabilize the aneurysm (Dacron graph)
  115. Why might surgery not be done for aneruysm?
    may have hypertension and atherosclerosis

    will have bad outcome
  116. Pt teaching with untreated aneurysm?
    1. come in q 6 mo for ultrasound
  117. Dx of aneurysm?
    ultrasound, echo, CT, MRI
  118. Dissection?
    a life threatening condition where a longitudinal tear in the intimal layer of the vessel or separaion of the vessel wall occurs & involves hemorrhaging into the vessel wall and creating a blood-filled cavity -
  119. S/S of abd aortic aneurysm?
    • 1. pulsatile mass at umb
    • 2. mid mild abd pain
    • 3. lumbar discomfort due to enlargement pressing on a nerve - dissecting triple A will cause back pain
    • 4. stasis of blood may cause thrombosis
  120. Important consideration when a pt comes back from surgery for aneurysms?
    must watch for clots

    I&O if above renal artery - have a urometer in the foley bag
  121. 2 most common causes of aortic aneurysm?
    • 1. atherosclerosis
    • 2. degeneration of vessel media
  122. after age 50 more in men than in women
  123. 2 causes of abd aortic aneurysms?
    • 1. atherosclerosis
    • 2. hypertension
  124. Who gets dissection most?
    men 40-60 yrs with Hx of hypertension or in younger ppl with conn. tissue diseases
  125. S/S of dissection?
    • 1. excruciating pain that is tearing or ripping feeling
    • 2. BP usually moderately elevated
    • 3. in late stages BP will drop due to blood loss
  126. Dx of dissection?
    • 1. TEE
    • 2. history
    • 3. phys exam
    • 4. CT scans
    • 5. MRI
  127. TEE?
    transesophageal echo

    numb throat and shine light down esophagus to view the chambers of the heart and watch pumping and valves

    must be NPO before and after until gag reflex is good
  128. MAP?

    mean arterial pressure - avg pressure in the arterial system during ventricular contraction and relaxation and is a good indicator of tissue perfusion

    90-100 mmHg
  129. Tx for dissection?
    • BP control
    • monitor for S/S of hypvolemic shock
  130. The systolic and diastolic components of blood pressure are det by the ____ ____ & the ___ ____ _____.

    Formula for BP?
    CO & peripheral vascular resistance

    BP = CO X PVR
  131. What determines peripheral vascular resistance?
    radius of the arterioles
  132. Patho of neural regulation of BP?
    stimulation sent to cardiovascular center in the lower pons and medulla where info is integrated -> autonomic NS stimulation to maintain homeostasis

    PNS - impulses to heart through vagus nerve
  133. Baroreceptors?
    pressure sensitive receptors located in the walls of blood vessels and the heart
  134. 5 Factors involved in short-term regulation of BP?
    • 1. ANS stimulation
    • 2. barorecptors
    • 3. arterial chemoreceptors
    • 4. RAAS
    • 5. vasopressin/ ADH
  135. Arterial chemoreceptors function?
    sense drop in O2 and cause widespred vasoconstriction -> increases BP
  136. ADH AKA?

    Where is it released from and what is its function?
    ant pit - vasoconstrictor
  137. Long term regulator of hypertension?
    kidneys regulate with higher level of Na and water elimination
  138. Essential hypertension?

    genetic hypertension that doesn't need Dx test to diagnose it - can Dx with family Hx and phys exam

    may do Dx test if adopted and don't know family Hx

    primary hypertension
  139. Most common type of HTN?
    primary/essential - cause unknown - genetic
  140. Racial groups with higher HTN?
    AA and more severe HTN

    not responsive to BP meds
  141. Risk factors for primary HTN?
    • 1 family Hx of HTN
    • 2. race - AA
    • 3. age
    • 4. T2DM
    • 5. hyperlipidemia
    • 6. obesity
    • 7. metabolic syndrome
  142. What is the key to reducing probs from HTN?
    early DX and intervention
  143. Lifestyle factors for HTN?
    • 1. gigh Na intake
    • 2. excessive calorie intake
    • 3. obesity
    • 4. phys inactivity
    • 5. excessive alcohol consumption
    • 6. sleep apnea
  144. Metabolic syndrome?
    high BP, obesity, high BG, & hyperlipidemia
  145. Manifestations of primary HTN?
    • 1. may be asymptomatic
    • 2. symptoms that may be present are r/t long-term effects of HTN on the organ systems of the body
  146. What may ppl be tested for if they have HTN?
    sleep apnea
  147. Organs effected by HTN?
    kidneys, heart, eyes, and blood vessels
  148. What lab to look at to det renal insufficiency?
  149. How does HTN affect the heart and the kidneys?
    increases workload on the left ventricle and causes renal insufficiency
  150. Dx of HTN?
    need at least 2 or more BP readings to Dx
  151. Lifestyle modifications to TX HTN?
    • 1. weight reduction
    • 2. regular phys activity
    • 3. reduce dietary NA intake
    • 4. moderation of alcohol intake
  152. Pharmacologic Tx of HTN?
    use a stepwise approach
  153. If a pt comes in with creatinine of 1.2, high BP, atherosclerosis, and admitted with chest pain.....

    What will the MD do?
    How will renal insufficiency affect the Dx done?
    usually will send for a heart cath

    if have renal insufficiency cannot give the dye for heart cath b/c damages kidney
  154. Major sequelae of HTN?
    renal insufficiency
  155. Nursing consideration if a pt is going to have a heart cath?
    make sure to check creatinine on labs and notify MD if it is abnormal - this is a nursing responsibility
  156. Secondary HTN?
    HTN caused by another disease process
  157. 3 EX of secondary HTN?
    • 1. renal hypertension
    • 2. disorders of adrenocorticosteroid hormones
    • 3. phenochromocytoma
  158. Can pt with renal insufficiency have heart cath?
    yes, but they need meds to protect their kidneys - mucomyst - tastes horrible
  159. Malignant HTN?
    secondary HTN accelerated and potentially fatal form
  160. Why is one BP reading not enough for DX?
    may have white coat syndrome
  161. Who is most at risk for malignant HTN?
    • 1. young AA men
    • 2. women with HTN of pregnancy
    • 3. ppl with renal and collagen diseases
  162. HTN meds?
    • 1. first choice diuretics - hctz
    • 2. add another drug
    • 3. add another drug of diff category (helps better than just increasing mg)
    • 4. will pick diff drugs for diff race b/c act diff
    • ----Ca channel blockers work better for AA
  163. Manifestations of malignant HTN?
    • 1. sudden marked elevations in blood pressure
    • 2. diastolic values >120mmHg
    • 3. HA
    • 4. restlessness
    • 5.confusion
    • 6. stupor
    • 7. motor and sensory deficits
    • 8. visual disturbances
    • 9. convulsions
    • 10. coma
  164. Action before giving a BP?
    check the BP!!!
  165. Serious complication of malignant HTN?
    hypertensive encephalopathy & BP
  166. Tx of malignant hypertension?
    give meds to lower BP - give them slowly to avoid sudden drop in BP
  167. Why must BP meds be given slowly if a pt has extremely high BP?
    will bottom out BP & can cause strokes
  168. What occurs in orthostatic HTN?
    abnormal drop in BP upon sitting up or standing that also causes increase in heart rate
  169. S/S of orthostatic HTN?
    • 1. tachycardia
    • 2. dizziness
    • 3. syncope - fainting
  170. What is a common cause of orthostatic HTN?

    Who is most at risk for it?
    any anti-HTN drug can cause it

  171. 6 things that can cause orthostatic HTN?
    • 1. reduced blood volume
    • 2. drug-induced HTN
    • 3. aging
    • 4. bed rest and immobility
    • 5. disorders of ANS function
    • 6. dehydration or too much dialysis
  172. How can the nurse test to see if pt has orthostatic HTN?

    Why might this be ordered?
    do orthostatic BP readings

    if testing for dehydration or too much dialysis
  173. Varicose veins?
    dilated or tortuous veins of the lower extremities which can lead to venous insufficiency
  174. 8 causes of varicose veins?
    • 1. impaired flow in deep venous channels
    • 2. DVT
    • 3. pressure on abd veins caused by obesity
    • 4. tumor
    • 5. pregnancy
    • 6. standing position
    • 7. heavy lifting
    • 8. incompetent valves
  175. Dx of varicose veins?
    • 1. visualization
    • 2. doppler ultrasound flow
    • 3. angiograph
  176. Who is varicose veins more common in?
    • 1. over 50 years old
    • 2. family Hx exp in women
    • 3. nurses - standing a lot
  177. S/S of varicose veins?
    • 1. unsightly appearnace
    • 2. aching in the lower extremities
    • 3. edema
  178. Way to prevent varicose veins?
    compression stockings
  179. Tx of varicose veins?
    • 1. elastic support stockings
    • 2. sclerotherapy
    • 3. surgical treatment
  180. Chronic venous insufficency?
    valve leaflets damaged rendering them incapable of closure - emptying of deep veins cannot occur
  181. S/S of chronic venous insufficency?
    • 1. tissue congestion
    • 2. edema
    • 3. brown pigmentatin of skin
    • 4. stasis dermatitis
    • 5. stasis or venous ulcers
  182. Where are venous ulcers usually located?
    over the ankle and lower leg due to chronic venous HTN
  183. Vircows Triad?
    S/S that occur in chronic venous insufficiency

    • 1. stasis of blood - immobility
    • 2. vessel wall injury - trauma and surgery
    • 3. increased blood coagulabiluty - use of oral contraceptives
  184. Vircows Triad?
    • 1. 50% are assymptomatic
    • 2. fever
    • 3. malaise
    • 4 elevated WBC
    • 5. elevated sedementation rate
    • 6. positive Homan's sign
  185. Venous thrombosis prevention?
    • 1. early abulation
    • 2. support stockings
    • 3. sequential pneumatic compression device
    • 4. prophylactic anticoagulation
    • 5. ankle flexion & extension **
  186. Dx of venous thrombosis?
    • 1. venography
    • 2. ultrasonography
    • 3. D-dimer
  187. S/S of venous insufficiency in legs?
    • 1. edema severe
    • 2. will have pulses
    • 3.
  188. Pericardial effusion?
    accumulation of fluid in the pericardial cavity due to injury,
  189. Why do pt need to flex and extend ankle after surgery?

    What is it imp to teach them?
    blood flow

    why they need to do this and other things so they will comly
  190. What does a positive D-dimer mean?
    means pt is at risk for blood clots but not that they have them
  191. If pt has a swollen extremity should they get up?

    If 1 leg is swollen really badly should it have TED and compression applied?

    What about other leg?
    shouldn't get up

    no TEDs and Kendalls on swollen leg

    other leg - yes
  192. Cardiac tamponade?
    life-threatening,slowing of the heart due to rapid compression of the heart due to the accumulation of lfuid, pus, or blood in the pericardial sac r/t trauma, cardiac surgery, cancer, or uremia
  193. S/S of cardiac tamponade?
    decreased CO and bradycardia
  194. Dx of cardiac tamponade?
    key to Dx ***pulsus paradoxus - drop in BP when pt takes a breath
  195. What will occur if the pericardial effusion becomes excessive?
    fluid will keep heart from filling during diastole

    cardiac tamponade
  196. Pericardiocentesis?
    pull fluid off pleural effusion
  197. Biggest issue with cardiac tamponade?
    decreased CO
  198. Why does pulsus paradoxis occur?
    So much fluid in thoracic cavity, when take a breath there is too much pressure in there and BP drops
  199. Acute pericarditis?
    inflammation of the pericardial sac due to viral infections, after cardiac surgery, connective tissue disorders
  200. What Dx test will show pleural effusion and cardiac tamponade?
    echocardiogram  ECG
  201. What is a pt at risk for after cardiac surgery?
    acute pericarditis
  202. Who has more acute pericarditis?
    more in men than women
  203. Tx for acute pericarditis?
    usually take ASA & naproxen/aleve and send home

    depends on causative agent
  204. S/S of acute pericarditis?
    • 1. chest pain
    • 2. pericardial friction rub
    • 3. EKG changes
    • 4. pain relieved by sitting up and leaning forward and slow shallow breaths
  205. Dx of acute pericarditis?
    • 1. clinical manifestations
    • 2. chest X-ray
    • 3. ECG
    • 4. echo
  206. Coronary Heart Disease?

  207. CAD - coronary artery disease
  208. Left main coronary artery?
    left anterior descending that feeds blood to left ventricle and the circumflex branches
  209. Right coronary artery?
    feeds blood to back of heart, SA and AV nodes
  210. #1 cause of coronary heart disease?
    atherosclerosis - obesity, smoking, DM, hypertension, high cholesterol
  211. RCA?
    right coronary artery
  212. If someone comes to the ER with chest pain what will be done and why>?
    12 lead ECG- to show if there are probs and where they may be located:  can show if RCA or left coronary artery is blocked, etc
  213. What will occur if RCA is blocked?
    firing of SA node can be interrupted b/c ischemia to this area can kill SA node and they will have to have a pacemaker
  214. LAD?
    left anterior descending coronary artery
  215. Where do lesions in CHD usually occur?
    first usually several cm of LAD & L circumflex or the entire length of RCA
  216. Stable plaque?
    plaques that contain a lot of collagen and fibrous conn tissue that makes it less likely to rubture - obstructs blood flow
  217. Stable angina?
    angina that is precipitated by increase work demands of the heart and can be aleviated with rest

    will occur with phys exertion, exposure to cold, and emot distress
  218. 3 characteristics of unstable angina?
    • 1. occurs at rest and lasts more than 20 minutes
    • 2. it is severe and described as frank pain of new onset
    • 3. it occurs with a pattern that is more severe, prolonged, and frequent
  219. Acute myocardial infarction?

    What will pt complain of?
    ischemic death of myocardial tissue

    • C/O:
    • 1. severe pain
    • 2. crushing pain - sitting on chest
    • 3. may radiate to L arm, neck, and jaw
    • 4. NV
    • 5. not relieved by rest or sublingual nitroglycerin
  220. Prinzmetal angina?

    AKA?  AKA?
    spasms of the coronary arteries that occur during rest

    variant or vasospastic angina
  221. Tx for prinzmetal angina?
    Ca channel blockers
  222. Medication for arterial spasms?
    Ca channel blockers
  223. Unstable plaque?
    can rupture and cause platelet adhesions & thrombus formation

    platelet adhesions- fatty plaque covered in fibrin
  224. What occurs after a plaque ruptures?

    • inflammatory response -> block artery completely
    • clot busters
  225. Time for Tx with MI?
    within 6 h
  226. Stable angina main teaching?
    if normal pain changes in any way need see/call MD - can mean blockage is worse
  227. Who commonly presents differently with MI pain?
    women & DM - NV, back pain, jaw/tooth pain

    DM pt - have neuropathy
  228. Dx of acute MI?
    1. EKG changes - T-wave inversion, ST segment depression or elevation & dev of Q-wave

    2. serum markers:  myoglobin, creatine kinase MB (CK-MB), troponin I & triponin T
  229. NSTEMI?
    non Q-wave MI
  230. Tx for MI?
    MONA - morphine, oxygen, nitro, aspirin (chewed)

    also - analgesic agents, B-adrenergic blockers(block EPI & NE), nitrates

    thrombolytics and revascularization need to be initiated within 60-90 min of onset of symptoms
  231. STEMI?
    Q-wave MI
  232. ROMI panel?
    rule out MI
  233. What will be done with MI S/S?
    12 lead ECG to see if any ST elevation & ROMI panel
  234. If see ST elevation of ECG what is it
  235. If have ST elevation of 12 lead but have labs that show MI what is it?
  236. Interpreting ECG and ROMI panel?
    if have elevated ST will also have increased triponin = STEMI

    If don't have elevated ST but have increased triponin = NSTEMI
  237. Triponin?
    enzyme released from heart muscle when it is damaged

    the the higher triponin = more damage to heart muscle
  238. STEMI or NSTEMI worse?
  239. Tomb stoning?
    QRS complex elevated so much it looks like a tomb stone with ST elevation
  240. 8 complications of MI?
    • 1. sudden death
    • 2. heart failure
    • 3. cardiogenic shock
    • 4. pericarditis
    • 5. thromboemboli
    • 6. rupture of the heart
    • 7. ventricular aneurysms
    • 8. may see increased temp due to necrotic tissue
    • 9. arhythmias
  241. What may occur several days after an MI?
    pt may spike fever r/t inflammatory response to necrotic tissue - still need to contact MD
  242. Cardiogenic shock?
    decreased circulation of blood due to heart failure
  243. Why is triponin main protein for MI?
    myoglobin & CK-MB will be released with ANY muscle damage

    triponin is heart muscle specific
  244. Cardiomyopathy?
    deterioration of the heart muscle
  245. Dilated cardiomyopathy?
    progressive cardiac hypertrophy and dilatin and impaired pumping ability of 1 or both ventricles due to alcohol abuse, drug abuse, or genetic - have a gigantic heart
  246. S/S of dilated cardiomyopathy?
    • 1. heart failure/CHF S/S:
    • 2. EF 40% or less- ejection fraction (decreased L ventricle function)
    • 3. dyspnea on exertion
    • 4. paroxysmal nocturnal dyspnea - suddenly feel like can't breathe in middle of night
    • 5. orthopnea (orthopnea X5 = need 5 pillow to prop up)
    • 6. fatigue
    • 7. ascites
    • 8. peripheral edema
    • 9. S3 or S4
    • 10. ventricular arrhythmias
    • 11. thrombus
  247. Dx of dilated cardiomyopathies?
    echo, chest Xray, TEE (transesophageal), cardiac cath
  248. Tx of dilated cardiomyopathy?
    • 1. digitalis to increase contractility
    • 2. decrease workload of heart - decrease preload and afterload -> increases CO
  249. Cardiomegaly?
    enlarged heart
  250. Infective endocarditis?
    uncommon, life-threatening infection of the endocardial surface of the heart and valves - may see vegetations on the valves
  251. What does ejection fraction tell?


    Lower than ____ = heart transplant.
    how well left ventricle is working

    normal is in 50's

    lower than 20 = heart transplant
  252. How to get pt EF?
    will show on echo/ECG
  253. 2 factors in infective endocarditis?
    1. a damaged endocardial surface & portal of entry by which the organism gains access to the circulatory system

    2. presence of valvular disease, prosthetic heart valves, or congenital heart defects provides an env conductive to bacterial growth
  254. If echo and heart cath have an EF on them which report is more accurate?
    cardiac cath report
  255. If MD wants to know what the L ventricular function is what will you tell them?
    the EF of the pt
  256. Decrease preload/afterload?
    • 1. ACE inhibitors
    • 2. diuretics
    • 3. dangling legs
  257. Ppl with valvular probs are at risk for what?

    infective endocarditis when have teeth cleaned b/c blood from teeth will take bacteria to the heart

    may give prophylactic ABX before and after dental cleaning to prevent it
  258. What type of pt may need to have prophylactic ABX with dental cleanings?

    What other times may this be necessary?
    pt with valvular probs:  valve replacement, congenital valve probs

    surgery, urology procedures
  259. What test shows vegetation on a valve?
  260. S/S of infective endocarditis?
    • 1. fever & S/S of infection
    • 2. petechial hemorrhages causes by vegetations breaking off
  261. Pt teaching with valve probs?
    take ABX before and after dental cleaning
  262. Dx of infective endocarditis?
    blood cultrues, echo, TEE
  263. Tx of infective endocardits?

    Is Tx started before or after blood cultures are done?
    antibiotic therapy

    blood cultures should be drawn first - make sure that this gets done - may start ABX before returned but must be drawn to get accurate data
  264. Rheumatic heart disease?
    acute, immune-mediated, multisystem inflammatory disease following a group A B-hemolytic strep throat infection - causes valvular probs
  265. When does rheumatic heart diasease usually occur?
    about 1-4 weeks after strep infection
  266. How can rheumatic heart disease by prevented?
    ABX can prevent the strep from damaging the valves of the heart
  267. What MO causes rheumatic heart disease?
    group A - Bhemolytic strep
  268. What should be done if suspect a pt has rheumatic heart disease?
    • 1. ask if they have had sore throat
    • 2. draw labs- anti-streptolysin O titer
  269. Test that will show that a pt has had a strep infection?
    antistreptolysin O titer is positive
  270. Dx of rheumatic heart disease?
    • 1. echo
    • 2. sed rate
    • 3. C-reactive protein
    • 4. TEE
    • 5. antibiotics
    • 6. positive strep titer)
  271. Age most rheumatic fever occurs in?
    children 5-15
  272. What is most often affected by rheumatic heart disease?
    mitral and aortic valves
  273. Tx of rheumatic heart disease?
    anti-inflammtory drugs
  274. If a pt has had RHD what are they now at risk for?

    infective endocarditis b/c they may have sustained valvular damage
  275. Will a person with rheumatic heart disease have a positive throat culture for strep?
    probably not- usually already gone
  276. Stenosis?

    narrowing of the valve orifice and failure of the valve leaflets to open normally

    valve is closed when it should be open

    2 causes:  may be born with stiff valve or can be RHD
  277. Mitral stenosis?

    What may cause it?
    narrowing of the mitral valve that causes left atrium enlargement

    can be caused by RHD
  278. If a person has RHD when may they start to have probs?
    as they age may have more valve probs and need valve replacement
  279. Why may left atrium enlarge?
    if mitral stenosis occurs can cause left atrium to have extra work getting blood through
  280. Aortic stenosis?

    narrowing of the aortic valve that causes it to be closed during systole when it should be open

    RHD or Ca depositis that occur as age (elderly)
  281. Who is at risk for aortic stenosis?
    person who had RHD and the elderly
  282. What occurs with aortic stenosis?
    enlarged L ventricle due to increased work to get blood through aortic valve

    will eventually cause L-sided heart failure -> may have to have surgery to prevent this
  283. Incompetent/regurgitant valve?
    permits backward flow to occur when the valve should be closed

    open when should be closed
  284. What can occur with regurgitating valve?
    increased workload for the heart r/t having to repump regurgitated blood
  285. Causes of regurgitating valves?
    RHD or congenital
  286. MVP?

    Who does it usually occur in?
    mitral valve prolapse - form of rugurgitating valve

    usually occurs in young women
  287. Cause of mitral valve regurg?


    enlarged L atrium b/c  blood comes back into atrium during systole and has to be pumped back into ventricle
  288. Cause of aortic valve regurg?


    L ventricular failure b/c blood goes into aortic valve and blood goes back into the L ventricle to be repumped
  289. Who has mitral valve prolapse most?
    women and genetic / in families
  290. S/S of mitral valve prolapse?
    • 1. tachycardia
    • 2. palpitations especially under stress
  291. #1 thing need to ask person with heart palpitations?

    What else do you need to ask?
    How may the this be treated?
    ask about diet: 

    any caffeine/energy drinks

    Ask about stress also:  if under a lot of stress may need a B-blocker until stress is alleviated
  292. What should be eliminated from diet of cardiac pt esp pt with arrhythmias/palpitations?
    caffeine, alcohol, and cigarettes
  293. CO?
    cardiac output - amnt of blood the heart pumps each minute - normally 8L/min
  294. Preload?
    reflects the loading condition of the heart a the end of diastole

    shows venous return to the heart
  295. Afterload?
    represents the force that the contracting heart must generate to eject blood from the filling heart - systemic vascular resitance
  296. Cardiac contractility?
    mechanical performance of the heart
  297. Increased preload affect on heart failure?
    will increase work of heart even more if preload is higher
  298. If vasoconstrict how will this affect preload?


    How is this treated?
    will increase preload and afterload

    give ACE inhibitors

    may dangle legs before meds are started
  299. What position should pt with heart failure not be in?
    laying flat - they will feel like they are drowning
  300. What drug helps strengthen contractility of heart muscle?

    Side effect?

    will decrease heart rate
  301. Compensatory mechanisms of heart failure?
    • 1. Frank-Starling mechanism - heart muscle stretches -> remodeling -> heart failure b/c stretching causes permenant damage and muscle won't go back (loses elasticity)
    • 2. sympathetic nervous system
    • 3. RAAS
    • 4. natriuretic peptides
  302. 4 causes of heart failure?
    • 1. acute MI
    • 2. hypertension
    • 3. cardiomyopathy
    • 4. renal failure
  303. 2 types of heart failure?
    right and left sided
  304. 3 causes of L sided heart failure?
    • 1. AMI - acute MI
    • 2. valvular defects - mitral or aortic stenosis/regurg
    • 3. hypertension - resistance in the vessels increases workload on heart -> heart failure
  305. AMI?
    acute MI
  306. Dx of L sided heart failure?
    • 1. S/S
    • 2. history and physical
    • 3. lab- BNP - brain natriuretic peptid - shows ventricular failure
    • 4. EKG
    • 5. chest x-ray
    • 6. echo
  307. S/S of L sided heart failure?
    • 1. decreased CO
    • 2. pulmonary congestion:  crackles (air moving through water), will see on Xray
    • 3. orthopnea
    • 4. frothy pink sputum
    • 5. paroxysmal nocturnal dyspnea
    • 6. fatigue
    • 7 dyspnea on exertion
  308. 3 causes of R sided heart failure?
    • 1. L sided failure
    • 2. pulmonary disease -COPD (not pulm congestion like left sided failure)
    • 3. Cor pulmonale - increased R ventricle side due to chronic pulmonary hypertension
  309. Cor pulmonale?
    enlargement & failure of R ventricle due to pulmonary hypertension
  310. What is the one diagnosis that can cause R sided heart failure?
    COPD - blue bloater
  311. Chest Xray with L sided heart failure?
    will show pulmonary congestion
  312. What does BNP indicate?
    ventricular function - if it starts to go down means they are improving
  313. Pulmonary congestion, crackles/rales, O2 sat low, pink/frothy sputum?
    L sided heart failure
  314. Person thinks have heart failure what will be done?

    As get better what will occur?

    BNP will go down
  315. Why does L failure cause R failure?
    because L causes fluid to back up to lungs then backs up to R ventricle -> increases work of R ventricle - R sided failure
  316. If a pt has Hx of COPD and are swollen what type of heart failure prob have?
    R sided
  317. S/S of R sided heart failure?
    • blood backs up everywhere in body and fluid escapes everywhere
    • 1. peripheral edema (3+, 4+, extreme)
    • 2. GI congestion - blood backs up in GI tract
    • 3. liver congestion & hepatomegaly
    • 4. ascites
    • 5. splenomegaly
    • 6. JV distention
  318. Pt with peripheral edema, hepatamegaly, spleanamegaly, & ascites?
    R sided heart failure
  319. Goals of heart failure Tx
    relieving symptoms and improving the quality of life with long-term goal of slowing, halting, or reversing cardiac dysfunction
  320. Tx of heart failure?
    • 1. decrease preload
    • 2. decrease afterload
    • 3. increase contractility
    • 4. possible fluid restriction
    • 5. salt restriction
    • 6. weigh daily
    • 7. drugs - diuretics, digoxin, ACE inhibitors, beta blockers
  321. Acute pulmonary edema?
    accumulation of fluid in lungs
  322. S/S of acute pulmonary edema?
    • 1. SOB
    • 2. cyanosis
    • 3. tachycardia
    • 4. cool
    • 5. frothy, pink sputum
    • 6. crackles
    • 7. pt will want to sit up, restless, anxious
  323. 4 Tx of acute pulmonary edema?
    • 1. digoxin
    • 2. diuretics
    • 3. vasodilators
    • 4. O2
    • 5. may need face mask or mechanical ventilation
  324. 3 stages of shock?
    • 1. nonprogressive stage in which the normal compensatory mechanisms prevent large changes in circulatory function
    • 2. progressive state, in which the shock becomes progressively worse
    • 3. irreversible stage in which the shock has progressed to such an extent that all forms of therapy  are insufficient to save the person's life
  325. Cardiogenic shock?
    failure of heart to pump
  326. Beta blockers contraindicated in ______ but can be given slowly once they are improving and will help over time.
    Congestive heart failure
  327. Most common cause of cardiogenic shock?
  328. What happens to cardiogenic shock pt BP?

    Do we give them fluids?
    BP drops

    no fluid- heart not pumping so won't do any good
  329. Tx for cardiogenic shock?
    • 1. decrease workload of heart
    • 2. O2
    • 3. vasodilators ?
    • 4. vasoconstrictors
    • 5. aortic balloon pump
  330. What should not be done with cardiogenic shock to raise BP?
    do not give fluids to raise BP
  331. Hypovolemic shock?
    diminished blood volume
  332. Causes of hypovolemic shock?
    • 1. hemorrhage
    • 2. severe burns
    • 3. vomiting or diarrhea
  333. S/S of hypovolemic shock?
    • 1. thirst
    • 2. tachycardia
    • 3. cool and clammy skin
    • 5. decreased UO
    • 6. restlessness
    • 7. can lead to apathy
    • 8. stupor and coma
  334. Drugs for cardiogenic shock?
    1. vasoconstrictors - dopamine, levafed
  335. Major side effect to look for with major vasoconstricting drugs?
    necrotic tissue in extremites r/t decreased blood flow
  336. Tx of hypovolemic shock?
    • 1. treat cause
    • 2. O2
    • 3. fluids
    • 4. blood
    • 5. vasoconstrictors
  337. If pt has not been typed and cross matched but needs blood what can be done?
    give them O-
  338. Distributive shock?
    fluid shifts out of vessels:  char. by loss of blood vessel tone, enlargement of the vascular compartment, and displacement of the vascular volume away from the heart and circulation
  339. 3 types of distributive shock?
    • 1. neurogenic shock
    • 2. anaphylactic shock
    • 3. septic shock
  340. 5 complications of shock?
    • 1. acute resp distress syndrome
    • 2. acute renal failure
    • 3. GI complications
    • 4. DIC
    • 5. multiple organ dysfunction syndrome -MODS
  341. 2 types of shocks that would give fluid to?

    What type don't give fluid to?
    distributive and hypovolemic

    cardiogenic shock
Card Set:
patho 4 CV - Vickers
2013-04-09 16:05:21
cardiovascular nursing

CV for patho test 4 Vickers
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