cardiac 2

Card Set Information

Author:
Anonymous
ID:
8172
Filename:
cardiac 2
Updated:
2010-02-27 10:20:49
Tags:
cardiac 2
Folders:

Description:
cardiac 2
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user Anonymous on FreezingBlue Flashcards. What would you like to do?


  1. sodium (Na+)
    low or high levels of this do not directly affect cardiac function
  2. hyponatremia
    decreased sodium levels indicate fluid excess and can be caused by HF or administration of thiazide diuretics
  3. hypernatremia
    increased sodium levels indicate fluid deficits and can result from dec. water intake or loss of water through excessive sweating or diarrhea
  4. potassium (K+)
    has a major role in cardiac electrophysiologic function
  5. hypokalemia
    • decreased potassium levels due to administration of potassium excreting diuretics
    • can cause many forms of dysrhythmias, including life-threatening ventricular tachycardia or ventricular fibrillation, and predispose pts taking digitalis to digitalis toxicity
  6. hyperkalemia
    • increased potassium levels increased potassium levels can result from an increased intake of potassium-e.g. foods high in potassium or potassium supplements, dec. renal excretionof potassium, use of potassium-sparing diuretics-e.g. spironaldactone, or use of angiotensin converting enzyme inhibitors (ACE inhibitors) that inhibit aldosterone function
    • serious consequences include heart block, asytole, and life-threatening vent. dysrhythmias
  7. calcium (Ca+)
    necessary for blood coaguability, neuromuscular activity, and automaticity of the nodal cells (sinus and atrioventricular nodes)
  8. hypocalcemia
    • dec. calcium levels slow nodal function and impair myocardial contractiltiy
    • the latter effect increases the risk of HF
  9. hypercalcemia
    • increased calcium levels can occur with the administration of thiazide diuretics b/c these medications reduce renal excretion of calcium
    • potentiates digitalis toxicitym causes inc. myocardial contractility, and inc. the risk for varying degrees of heart block and sudden death from ventricular fibrillation
  10. magnesium (Mg+)
    • necessary for the absorption of calcium and metabolism of adenosine triphosphate
    • it plays a major role in PRO adn CHO synthesis and muscular contraction
  11. hypomagnesemia
    • decreased levels are due to enhanced renal excretion of this from the use of diuretic or digitalis therapy
    • low levels predispose pts to atrial or ventricular tachycardias
  12. hypermagnesemia
    • increased levels are commonly caused by the use of cathartics or antacids containing magnesium
    • increased levels depress contractility and excitability of the myocardium, causing heart block and, if severe, asytole
  13. BUN & CRT
    • end products of PRO metabolism excreted by the kidneys
    • elevated levels indicate reduced renal perfusion from dec. CO or intravascular fluid volume deficit as a result of diretic therapy or dehydration
    • both lab values are used to assess renal function, although CRT is a more sensitive measure, renal impairment is detected by an increase in both
    • normal CRT level and elevated BUN detect an intravascular fluid voolume deficit
  14. glucose
    • elevated in stressful situations, when mobilization of endogenous epinephrine results in conversion of liver glycogen to glucose
    • serum glucose levels are drawn in a fasting state
  15. PTT/aPTT
    • measures the activity of the intrinsic pathway and is used to assess the effects of unfractionated heparin
    • therapeutic range 1.5-2.5 times the baseline values
    • adjustment is required for aPTT <50 sec.-inc. dose, or >100 sec.-dec. dose
  16. PT
    measures the extrinsic pathway activity and is used to monitor the level of anticoagulation with Warfarin (Coumadin)
  17. INR
    • reported with the PT
    • provides a standard method for reporting PT levels and eliminates the variation of PT results from different laboratories
    • this, rather than the PT alone, ios used to monitor the effectiveness of Warfarin
    • therapeutic range-2.0-3.5, although specific ranges vary based on diagnosis
  18. CBC
    • identifies the total number of white and red blood cells and platelets, and measure Hgb AND Hct
    • the CBC is carefully monitored in pts with cardiovascular dx
  19. WBC
    monitored in immunocompromised pts, including pts with heart transplants or in situations where there is a concern for infection-e.g. after invasive procedures or surgery
  20. Hgb and Hct
    • represents the percentage of rbcs found in 100 ml of whole blood
    • the rbcs contain Hgb and Hct levels, and have serious consequences forpts with cardiovascular disease, such as more frequent angina or acute myocardial infarction
  21. platelets
    • first line of protection against bleeding
    • once activated by blood vessel wall injury or rupture of atherosclerotic plaque, platelets indergo chemical changes that form a thrombus
    • several medications inhibit platelet function, including ASA, clopidogrel (Plavix), ReoPro, and Integralin
    • when these meds are administered, it's essential to monitor for thrombocytopenia (low platelet counts)
  22. these are essential for proper cardiac function
    cardiac d/os and medications can alter e-lyte imbalance
    135-145=sodium

    3.5-5.1=potassium

    8.6-10.2=calcium

    1.8-2.6=magnesium
  23. potassium (K+)
    hypokalemia increases the risk of digitalis toxicity, ventricular dysrhythimias, hypokalemia from renal disease or excess potassium supplements can lead to ventricular dysrhythmias and asytole
  24. sodium (Na+)
    • hyponatremia with long term diuretic therapy
    • hypernatemia with excess IV saline infusion
  25. calcium (Ca+)
    • cardiac effects of hypocalcemia include ventricular dysrhythmias, prolinged QT interval and cardiac arrest
    • hypercalcemia shortens QT interval and causes AV block, digitalis hyposensitivity, and cardiac arrest
  26. magnesium
    cardiac effects of dec. magnesium include vent. tachcardia and fibrillation, while inc. magnesium causes dradycardia, hypotension, and prolonged QRS intervals
  27. serum lipid profile
    • a measurement to determine risk for atherosclerosis
    • includes total serum cholesterol (<200 mg/dl)
    • triglycerides 10-190 mg/dl), and lipoproteins
    • HDL-transport cholesterol to liver for excretion ("good cholrsterol"), 30-70 mg/dl
    • LDL-transport cholesterol to peripheral tissurs 9"ban cholesterol"), increases risk of heart disease, 130 mg/dl
  28. cardioversion and defibrillation
    • used to tx tachydysrhytmias by delivering an electrical current that depolarizes a criticaal mass of myocardial cells
    • when the cells repolarize, the sinus node is usually able to recapture its role as pacemaker

    one major difference btwn cardioversion and defibrillation is the timing of the delivered electrical current
  29. cardioversion
    • delivery of electrical current
    • is sychronized with the pts electrical events
  30. defibrillation
    • the delivery of the current is immediate and unsynchronized
    • after, resume CPR, check cardiac rhythm and deliver another shock if indicated
    • administer a vasoactive or antidysrhythmic ASAP after the rhythm check
    • after the event is complete, inspect the skin under the paddles for burns
  31. electrical cardioversion
    • involves delivery of a times electrical current to terminate a tachydysrhythmia
    • sycchronizes with ECG on a cardiac monitor so that the electrical impulse discharges during ventricular depolarization (QRS complex)
    • prevents discharge during vulnerable period of repolarization (Twave), which could result in VT or VFIB
  32. complications of pacemakers
    • local infection
    • bleeding and hematoma
    • hemothorax from puncture of subclavian or internal mammary artery
    • ventricular ectopy and tachycardia from irritation of ventriculaar wall by the endotrachial electrode
    • movement or dislocation
    • phrenic nerve, diaphoretic (hiccuping) or skeletal muscle stimulation if lead is dislocated
    • rarely cardiac tamponade following removal of epicardial wires used for temporary pacing
  33. endocardial pacer wires
    • threaded through a major vein into the right ventricle
    • can be temporary or permanent
    • can be hooked to a permanent generator
  34. epicardial pacer
    • lightly sutured to outside of heart and brought through chest wall
    • used in open heart surgery
    • temporary
  35. transcutaneous pacemaker
    • bradycardia
    • symptomatic but has a pulse
    • unresponsive to Atropine
    • needs emergency pacing
    • travels through skin
    • electrodes ant. and post.
    • if pt is alert, give sedation/analgesia
    • not indicated for pulseless bradycardia
  36. care of pacemaker
    • bradycardia and dec. CO indicate malfunction
    • analyze with ECG
    • may have to manipulate electrodes, change generator settings
    • stay away from strong electromagnetic fields
    • watch for dizziness, palpitations
    • hours after placement, watch for dislodgement
    • limit activity, immobilize extremity it was placed on
  37. ICDS
    • symptomatic recurrent medication
    • refractory AFIB
    • v. tach
    • v. dys.
    • has a generator and at least one lead
    • implanted like a pacemaker
    • responds to a rate that exceeds predetermined level and a change in isoelectric line segments
    • battery life is 5 yrs
    • can be used for bradycardia
    • complications-surgery related infection, equipment problems, premature battery depletion, dislodged or fractured leads
    • stay away rom magnetic fields
  38. nitroglycerin
    • dec. O2 consumption, inc. O2 supply
    • dec. ischemia
    • dec. pain
    • dec. preload
    • dec. CO
    • dec. BP
    • hold if BP is 90 or less systolic
    • can work as fast as 3 min.
  39. beta-blockers
    • dec. HR, dec. contractility
    • contraindications-hypotension, bradycardia, advanced atrioventricular block, decompensated HF, significant pulmonary obstructive disease-e.g. asthma
    • monitor EKG, BP
    • s/e-dec. libido, depression, fatigue, hypoglycemia
    • don't stop abruptly
  40. calcium channel blockers
    • may be used in pts who can't take beta-blockers or nitrates
    • prevent vasospasm
    • avoid with HF because dec. contractiltiy
    • s/e-hypotension, AV block, bradycardia, constipation, gastric distress
  41. antiplatelets/anticoagulants
    • ASA
    • Plavix/Ticlid-may replace ASA if allergic
    • heaprin
  42. ECG changes with an MI
    • T wave inversion
    • ST elevation in 2 leads
    • abnormal Q wave
  43. ACE inhibitors
    • dec. O2 demand
    • prevents remodeling
    • make sure pt is not hypotensive, hyponatremic, hypovolemic, or has hypokalemia b/f giving
    • monitor BP, UO, Na+, K+, and CRT closely
  44. pharmacologic therapy for MI
    • suspected MI
    • immediately treat with ASA
    • nitroglycerin, morphine, beta-blocker, and others as diagnosis is being confirmed
  45. thrombolytics
    • chest pain lasting linfer than 20 min, unrelieved by nitro
    • ST elevation in at least 2 leads facing same area of heart
    • < 6 hrs from onset of pain
    • contraindicated in:
    • active bleeding or bleeding d/o
    • hx or hemmorrhagic stroke, intracranial vessel formation
    • recent major surgery or trauma
    • uncontrolled HTN
    • pregnancy
    • avoid venipunctures and MI injections
  46. post CABG
    • pts normal stay in ICU is 5 days
    • home for extended care untio strong enough to go home
    • cardiac rehab consists of three stages and begins ASAP when pt is stable
    • the goals of cardiac rehab are to impreove the quality of life, limit the progression of the disease, and return to preillness lifestyle
    • although covered by most insurance, only 39% participate
    • stage 3 does not require supervision and is pt directed, so many "fall off the wagon"
  47. heart transplants
    • reserved for pts with end-stage cardiac disease
    • symptoms are uncontrolled with medical therapy and lack other surgical options
    • prognosis is less than 12 months to live
    • require immunosuppresive therapy to prevent the body from rejecting the heart, therefore, prone to infections
    • no nerve connections with sympathetic nervous system or vagus nerve
    • atropine and digoxine work work
    • pacemaker
  48. artificial hearts
    • replace pts own heart while waiting on a transplant
    • poor success rate
  49. pericarditis
    inflammation of the pericardial sac, the sac lubricates as the heart beats
  50. etiology of pericarditis
    • infections
    • acute MI
    • tumors
    • diseases
    • drug reactions
  51. cardiac tamponade
    • a build up of blood or other fluid in the pericardial sac
    • puts pressure on the heart, which may prevent it from pumping effectively
  52. clinical manifestations of pericarditis
    • chest pain with deep insoiration
    • dyspnea-comfortable sitting up and leaning forward
    • pericardial friction rub-you can hear it if they hold breath
    • ST elevation in all leads of the EKG
  53. diagnostic tests for pericarditis
    • H&P
    • EKG
    • echocardiogram
    • CT Scan
    • cardiac nuclear scan
  54. tx for pericarditis
    • tx the underlying cause
    • bedrest to rest the hear and dec. metabolic demands
    • ASA nsaids
    • steriods
    • ATBs for infections
  55. nursing diagnosis for pericarditis
    • pain
    • anxiety
    • dec. CO
  56. cardiac tamponade
    • rapid accumulation of fluid in the pericardial sac that compresses the heart and dec. ventricular filling and CO
    • can accumulate 50 ml of serous fluid up to 2,000
  57. etiology of cardiac tamponade
    • trauma
    • obstructed mediastinal tubes following CABG
    • pericarditis
  58. s/s of cardiac tamponade
    • tachycardia
    • apprehension
    • hypotension
    • muffled heart sounds/pericardial rub
    • decreasing UO
    • pulses paradoxous-arterial and pulmonary artery
    • waveforms > 10 mmHg (weaker pulse during inspiration and stronger pulse during expiration, should be opposite)
  59. tx for cardiac tamponade
    • pericardiocentesis-a pericardial needle w/ 50 cc syringe is used to aspirate fluid from the pericardial sac
    • monitor for dysrhythmias and ST elevation/changes
  60. outcome of cardiac tamponade
    • relieved if sx are relived immediately
    • BP increases
    • inc. in central venous pressure readings
  61. complications of cardiac tamponade
    • punture of the myocardium
    • dysrhythmias
    • recurrent tampoande-will have same sx
  62. shock
    a life threatening condition that causes inadequate perfusion that results in impaired cellular metabolism of all the organs in the body
  63. etiology of hypovolemic shock
    • lack of blood to supply oxygen and nutrients to the organs
    • hemmorhage is the most common cause-stop the bleeding
    • dehydration-replace fluids
    • third spacing-plasma expanders e.g. Albumin, Plasminaid
  64. etiology of cardiogenic shock
    • dec. contractility and CO
    • fail to meet the body's needs for O2 and nutrients
    • the most difficult type of shock to treat and has a mortality rate of 75-85%
    • chirf causes are AMI, dysrhythmias, and valvular disease-back up of blood, not going in the right direction
    • not enough blood to tissues
  65. etiology of septic shock
    • multiple organ dysfinction in response to an infection
    • most common cause of death in ICU, mainly from Gram Negative bacteria, then Gram Positive
    • nosocomial infections are a mojor cause of sepsis due to long hospital stays, invasive catheters and technology, surgical wounds, chronic diiseases, and cross contamination
  66. s/s of all 3 types of shock
    • early signs:
    • dec. LOC
    • tachycardia
    • rapid respirations

    • cool/pale skin, poor capillary refil-blood going to organs, not peripheral
    • dec. peristalsis and dec. bowel sounds
    • fatigue if not on Ativan drip
    • hypotension
    • dec. UO <30 ml/hr
    • fever-sepsis only
  67. diagnosis for shock
    • identify the cause
    • careful assessment of clinical sx and risk factors
    • labs-CBS, ABGs, liver enzymes
    • lactate levels correspond with degree of hypofusion
    • late indicator
    • EKG, CXR, echo, CT Scan
    • peritoneal lavage
  68. if she asks...
    blood cultures=septic

    enzymes=cardidogenic

    lytes=hypovolemic

    CBC=septic/hypovolemic
  69. tx for hypovolemic shock
    • treat the underlying cause
    • blood and/or fluid replacement-FFP, PRBCs, crystaloids/Albumin (to pull fluid back from peritoneal space and into blood vessel, bolus of Lactated Ringer's and NS then follow with the Albumin
    • PCWPgold standard tool to assess fluid regulation
    • monitor LOC, VS, PCWP, UO, and labs (CBC, cardiac enzymes to differentiatefrom cariogenic, e-lytes, BUN, CRT

    • fluids first if dehydrated
    • blood first if hemmorrhagic
    • fluids (crystlliods) and Albumin first if 3rd spacing, check liver enzymes
  70. hyypovolemic shock
    hypovolemia-cells in blood will be increased, sodium will be increased
  71. tx of cardiogenic shock
    • treat the cause
    • improve CO and dec. workload of the heart
    • thrombolytics, PTCA
    • administer intropic agents
    • reduce preload and afterload
    • IABP helps meet body's needs w/o inc. energy of the heart and increasing expenditure of O2, augments BP
    • need to go to cath lab
    • meds-Dibutamine increases CO w/o inc. HR and O2 requirements, metabolic won't increase either
    • Dopamine-supports BP, and increases blood volume (vasocontriction), perfuse kidneys. won't inc. HR
    • thrombolytics-know s/e and outcomes of meds
  72. septic shock
    • treat the cause of infection/Gram Negative bacteria, Gram Positive bacteria, viruses, fungi
    • IV fluid therapy-support BP
    • vasopressors after fluid therapy (eg. Dopamine-can use to support BP once fluid is restored, contraindicated in dehydration, never give in place of fluid resuscitation
  73. DIC
    • a coagulation d/o that uses up all of the clotting factors and forms multiple clots in the microcirculation that results in organ ischemia and necrosis because all the clotting factors are used up, the pt bleeds profusely
    • mortality rate is 80-90%
  74. etiology of DIC
    • occurs secondary to another cause
    • -sepsis
    • -trauma
    • -obstetrical conditions
    • -immune d/os
    • -malignancy
  75. clinical mainifestations of DIC
    • bleeding for an unknown reason
    • bleeding from all orifices and puncture sites
    • cyanosis in tips of digits and nose
    • dec. LOC
    • hypoxemia
    • dec. UO
  76. diagnostic testing for DIC
    • fibrin split products
    • fibrinogen levels decrease
    • ProTime and PTT decrease
    • D-dimer will be elevated, best test
  77. medical tx for DIC
    • treat underlying cause until the cause is treated, the DIC will persist
    • improve oxygenation
    • IV fluid replacement
    • correct e-lyte imbalances
    • administer vasopressors
  78. medical tx for DIC continued
    • Cryprecipitate to replace fibrinogen and clotting factors
    • FFP to replace clotting factors
    • heparin to interrupt and inhibit formation of emboli to help perfuse the organs
    • Amicar may be used with heparin-same effect
    • Xigris and antithrombin therapy (dec. inflammation and has an anticoagulation effect)
  79. complications of DIC
    • renal failure
    • gangrene
    • altered LOC
    • acute resp. distress syndrome-no exchange of O2 for waste products
    • MI
    • skin breakdown
  80. nursing dx for DIC
    • risk for deficient fluid volume
    • risk for impaired skin integrity
    • *ineffective tissue perfusion
    • death anxiety
  81. ventricular tachycardia
    • caused by an irritable focus in the ventricles
    • it fires at a rate of 150-250 bpm
    • override sites for control of heart

    • no P wave so no PR interval
    • wide QRS >.12
    • may be concious or unconscious
    • can turn into VFIB qquickly
    • cause-hypoxia, MI, angina, surgical procedures, cardiac cath
    • conscious with a pulse-tx with Lidocaine or Amiodarone bolus followed by a drip
    • unconscious and pulseless-CPR, defibrilate, ACLS protocol
  82. ventricular fibrillation
    • chaotic impulses that cause the heart to fibrillate
    • there is no cardiac muscular contraction

    • unconscious, no pulse, BP or respirations
    • Defibrillate, CPR, follow ACLS protocol
    • know Vasopression, epinephrine, Amiodarone, Lidocaine
    • cause-drowning, struck by lightening or electrical shock, hypothermia

    assess pt, check pulse, LOC, defibrillate, CPR-effective when a pulse is present, drugs won't make hypothermic, what caused this?
  83. asytole
    • cardiac standstill/flatline
    • there is no pulse, respirations, or BP
    • there is no electrical or mechanical activity of the heart
    • there are no complexes with this rhythm

    • the pt is clinically dead
    • tx-check rhythm in another lead, CPR, epinephrine, Atropine, pacing, intubate
    • how long has pt been like this?
    • assess for underlying cause, check leads, maybe in a real fine VFIB, pt is unconscious, no pulse, no BP, or respirations
    • CPR, Atropine (3mg total), epinephrine, external pacer, how long have they been like this? what's the cause?
    • intubate
  84. paced rhythm
    • paced rhythem with 1:1 capture
    • rhythem is regular
    • no P wave
    • pacer spike initiate QRS-takes place of P if no QRS-not capturing
    • pacer spike is on T wave-V tach
    • pacemakers used for 3rd degree heart block
  85. transvenous pacing
    • situations-pacemaker over a period of time, go to heart via the vein (Superior Vena Cava0
    • in ccath lab for example, used until you get a permanent pacemaker
  86. transcutaneous pacemakers
    • pad on front and back
    • situations-emergency (arrest, heart transplant, bradycardia, severe 3rd degree block)
  87. why we use pacemakers
    • don't have a rhythm that can perfuse tissues to meet needs (eg. bradycardia)
    • not enough CO to meet body's needs
  88. pericardial pacer wires
    situations-CABG, heart surgery
  89. nursing interventions with pacemakers
    • protect against micro-shock with all pacemakers
    • isolate wires, cut fingers out of a rubber glove and put over end of wires
    • used any time people won't respond to drugs

    if dislodged and goes into heart-can cause cardiac tamponade
  90. cardiovascular disease
    • leading cause of death in the US
    • formerly considered a disease of men -common in women
    • women with heart disease are still undertreated today
    • women do not receive appropriate follow up care
  91. s/s of chest pain in men
    • severe crushing chest pain that may radiate to arm or jaw
    • SOB and diaphoretic
    • N/V
    • heartburn
  92. s/s of chest pain in women
    • silent MI w/o pain
    • vague complaints of pain in arms, shoulders, or toothache
    • fatugue
    • N/V
    • heartburn
  93. protocol goals
    • identify AMI rapidly
    • minimize myocardial damage
    • preserve myocardial funtion
    • prevent complications
  94. diagnostic tests
    • HOPI-onset and current sx
    • AMPLER/medical and family HX
    • EKG and monitoring
    • cardiac enzymes, Troponin, CKMB
    • PT, PTT
    • BUN, CRT, lytes
    • CBC
    • CXRcath lab
  95. what to ask with cardiac pts and nursing interventions
    • when did the pain start?
    • what are the sx?
    • past medical and surgical hx?
    • VS
    • need 2 IVs
    • EKG-ist turn aroung test we can get (12 lead, compare, give to Dr.)
    • 0.1-1 ng WNL for Troponin (the best, increased for 1-2 wks) if Troponin is positive, do a CKMB-0-6%
    • BUN, CRT-to check renal function, because of contrast, use Mannitol which is a diuretic
    • CBC-baseline blood count of Hgb, HCT, platelets
    • CXR-to rule out other causes
  96. tx MONA
    • Morphine-decreases pain, dilates blood vessels, increases O2, decreases resp., dec. preload and afterload, dec. CO, Narcan to reverse
    • Oxygen-vasodilates, give 100%, inc. O2 to heart
    • Nitrogen-vasodilator, inc. O2, dec. BP, SL can take up to 3 in 5 min, can cause headache
    • Aspirin-dec. platelet aggregation, 325 mg, chew it
  97. ACS

    STEMI

    NSTEMI
    term used to describe unstable coronary disease or an evolving MI

    ST elevated myocardial infartion, indicates complete occlusion of a coronary artery

    non-ST elevated myocardial infartion indicates partial occlusion of a coronary artery
  98. detecting myocardial ischemia
    • anything larger than a small box=abnormal
    • anything amaller or less than a small box=normal
    • ST elevated=coronary artery occlusion
    • non-ST elevation=partial coronary artery occlusion
    • new Q waves and ST elevation=new onset left bundle block-impulse delayed throughout ventricle=new onset MI (in 2 leads)

    compare EKGs to determine if Q waves are new or old
  99. AMI interventions and thrombolytics
    • administered through peripheral IV (thrombolytics)
    • thrombolytics-lyse the clot
    • directly into coronary artery in CVL (thrombolytic)
    • complication:
    • hemmorhagic-caused by hemmorrhage (stroke)
    • thrombolytic-caused by clot (stroke)
    • hematomas
    • hemmorhage
    • impaired circulation
    • reperfusion dysrhythmias-ant. MI
    • heart blocks-inf. MI
    • tx and care:
    • avoid venipunctures and injections
    • ask if they've had recent surgery
    • blood work-platelets (150-400, cut off is 100,000, TPK, TNK)
    • Hgn, Hct
    • MONA
    • EKG
  100. percutaneous transluminal coronary angioplasty (PTCA)
    • invasive procedure performed under floroscopy
    • balloon tipped catheters flatten plaque against the artery wall
    • stents with cytotoxic drugs have greatly reduced reocclusion of the artery
    • platelet inhibitor derugs-ReoPro, Integralin
  101. post PTCA care
    • observe for acute closure-chest pain
    • coronary artery dissection
    • bleeding and circulation deficits
    • e-lyte imbalance
    • dysrhythmias
    • administers anticoagulants, nitrates, beta-blockers, ACE inhibitors
  102. beta-blockers
    • observe for hypotension, bradycardia
    • beta 2-can cause bronchospasms, for heart and lungs
    • beta 1-for heart cells
    • shouldn't be stopped abruptly-can couse MI

    remember lol or olol
  103. ACE inhibitors
    • cause peripheral vasodilation
    • dec. work of heart
    • *dec. remodeling and thinning of ventricle
    • observe for:hypotension, hypokalemia, Na+, K+, BUN, CRT, headaches, orthostatic hypotension
    • *prevents damage caused by dec. CO

    remember pril
  104. CABG
    • veins from legs of the internal mammary artery are used to bypass the obstructed vessels to restore circulation to the myocardium
    • improves quality of life and most pts remain pain free for 5 yrs
    • for in-stage disease
  105. post op CABG
    • monitor
    • ventilator (to conserve energy to heart), SaO2
    • ART line-monitoracurate BPs. blood gases
    • CVL-IV infusion
    • PCWP catheter-to measure pressures and fluid volume (pulmonary infarct is a complication)
    • chest tubes-monitor closely (output, type of drainage, ideal is less than 100 ml/shift, no leak)-CRX after to check for tube placement
    • IABP
    • pericardial pacer wires-in case of emergency
    • foley-monitor output, are kidneys perfusing
    • NG-air in stomach
    • hypothermia blanket-keep warm
    • insulin drip-catecholamine effect on BS, check qh
    • Ativan drip
    • Dibutamine-inc. CO w/o inc. HR
    • Dopamine-profuses kidneys
    • subject to e-lyte imbalances, give Ca+, K+, piggyback
  106. complications post CABG
    • assess for:
    • e-lyte imbalance
    • glucose levels
    • hypotension or hypertension
    • hypothermia
    • bleeding
    • dysrhythmias, MI, cardiac tamponade, cardiac arrest
    • altered LOC, stroke, seizures
    • pain
    • tension pneumothorax
    • infection
    • adverse reactions to drug therapy
    • assess for Dump-amt of blood released in chest tube when pt stands up after 6 hrs

What would you like to do?

Home > Flashcards > Print Preview