Cardiac Adv. Principles

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  1. What are the typical clinical manifestations of ischemic heart disease?
    Conventional ischemia (angina, MI, ischemic cardiomyopathy, sudden death)
  2. What are the three manifestations of ischemia that are more specific to cardiac surgery?
    Stunning, hibernation, ischemic conditioning
  3. What is the perioperative management of ischemia?
    • Pharmacologic manipulation of oxygen supply & demand through heart rate control & adequate coronary perfusion pressure
    • Inhibit thrombus formation on unstable plaque
    • IABP (intra-aortic balloon pump)
  4. Why do we use betablockers in ishemic heart disease?
    Avoid tachycardia-induced ischemia
  5. Why are there special considerations with impaired LV function?
    • BB have been shown to worsen outcome in patients with EF less than 35%.
    • Particularly pt w/irreversible decreases in EF.
  6. Nitrates are a cornerstone therapy for ischemic heart disease, what do they do?
    • Decrease myocardial O2 demand & increase supply via coronary vasodilation
    • Vasorelaxation of veins & large conduit arterial vessels
    • This decreased preload decreases anginal symptoms
  7. What % of patients with chest pain have syndrome x?
    Occurs in up to 20% of patients with chest pain
  8. What is syndrome x?
    • Anginal chest pain with normal coronary angiography & lack of extracardiac etiology of the angina
    • ? Coronary microvascular flow
    • Enhanced sensitivity of myocardial pain receptors
  9. What is the prognosis for patients with syndrome x?
    Same as the general population
  10. What is stunning?
    • Brief period of ischemia may lead to subsequent myocardial dysfunction for several hours.
    • It occurs during the reperfusion phase of ischemia reperfusion.
    • When we see it in heart surgery is following CPB, when the heart is reperfused it is said to be stunned myocardium.
    • Stunned myocardium is a less common manifestation of ischemia.
    • Not functioning correctly, wall motion abnormalities.
  11. What is hibernation?
    An area of myocardium adjacent to an area of infarction there’s impaired myocardial functions in the setting of impaired myocardial blood flow but it’s relieved following reinstitution of normal flow
  12. What is preconditioning?
    that brief intermittent period of ischemia confers protection against a subsequent larger ischemic insult
  13. What are the 2 major coronaries?
    RIGHT and LEFT Main
  14. How long is the LEFT main coronary?
    It ranges from a few millimeters to a few centimeters in length
  15. The left main coronary passes between the left atrial appendage and the pulmonary artery and generally divides into two branches, what are they?
    • Left anterior descending artery
    • Circumflex artery
  16. What part of the heart does the LAD perfuse?
    • Aka anterior interventricular artery
    • Delivers blood to portions of the left and right ventricles and much of the interventricular septum
    • The LAD travels down the anterior surface of the interventricular septum toward the apex of the heart
  17. Where does the left circumflex coronary go and what does it perfuse?
    • Travels in a groove called the coronary sulcus
    • This groove separates the left atrium from the left ventricle to the left border of the heart
    • It supplies blood to the left atrium and lateral wall of the left ventricle
    • Circumflex often branches to the posterior surfaces of the left atrium and left ventricle
  18. What are collaterals?
    Connections or anastomoses between two branches of the same coronary artery or connections of branches of the right coronary artery with branches of the left
  19. Where are collaterals common?
    Particularly common within the interventricular and interatrial septa, at the apex of the heart, over the anterior surface of the right ventricle, and around the sinus node
  20. Where does the right main coronary begin and where does it go from there?
    • Originates from an ostium behind the right aortic cusp
    • Travels behind the pulmonary artery, and extends around the right heart to the heart’s posterior surface, where it then branches to the atrium and ventricle
  21. Name the three branches right coronaries and where they perfuse
    • Conus: supplies blood to the upper right ventricle
    • Right marginal: traverses the right ventricle to the apex
    • Posterior descending branch: lies in the posterior interventricular sulcus and supplies smaller branches to both ventricles
  22. What things influence oxygen supply to the heart?
    • sympathetics (alpha and beta receptors)
    • vagus
    • systolic compression
  23. What things can influence oxygen demand?
    • hypoxia
    • acidosis
    • etc
  24. If you have a 100% increase in contractility (what the boxes are showing us) you have a _______% increase in O2 consumption.
    • 200% or more
    • As the heart gets more briskly contractile, as with an inotrope for example, the oxygen consumption goes up dramatically
  25. What things can oxygen consumption (in order from most to least)
    • contractility
    • heart rate
    • wall tension
    • muscle shortening
    • activation
    • (From slide 16 of lecture)
  26. What are the Chordae tendonae?
    The heart valve openings are guarded by flaps of tissue called leaflets or cusps that are attached to the papillary muscle by the chordae tindineae
  27. What are the papillary muscles??
    They are extensions of the myocardium that pull the cusps together and downward at the onset of ventricular contraction, thus preventing their backward expulsion into the atria
  28. So when someone has papillary muscle dysfunction then those leaflets would go back into the atria and you would see _______ _______ ________. The valve cusps move back into the atria during systole. Frequent problem when people have MV disease.
    systolic anterior motion
  29. Which valve has the largest diameters?
    The tricuspid opening has the largest diameter of all the heart valves
  30. What shape does the mitral valve look like? What special thing connects them??
    • Mitral valve resembles a cone-shaped funnel that extends into the cusps
    • These are connected by a fibrous tissue called the commissure
  31. Why do the tricuspid and mitral valves function as a unit (Mitral and tricuspid complex)?
    • because the atrium, fibrous rings, valvular tissue, chordae tindineae, papillary muscles, and ventricular walls are connected
    • Damage to any one of the complex’s six components can alter function significantly
  32. Tell me about the cusps of the pulmonic and aortic valves (which is thinner, what happens w/contraction & relaxation)?
    • Pulmonic cusps slightly thinner than aortic cusp
    • When ventricles contract, cusps behave like one-way valves
    • When ventricles relax, blood fills the cusps, closing them and preventing backflow
  33. What is SINGLE MOST COMMON CONGENITAL HEART LESION?
    Aortic Stenosis
  34. What is considered severe AS?
    • Stenosis is considered severe is the systolic gradient exceeds 50mmHg.
    • Or if the valve area is less than 0.8cm2.
  35. Why is atrial contraction so important in Aortic Stenosis?
    The LV is stiff and there is increased dependence on atrial contraction for filling the LV.
  36. What three things are essential in HD management of AS?
    • Normotensive
    • SR (need the atrial kick)
    • and adequate volume
  37. Why is hypotension in AS so bad?
    • Because the coronary arteries are filled from the aortic root. So if you don’t have enough pressure in aorta, the coronaries aren’t filled as well, particularly if you have a hypertrophied LV.
    • Aortic Stensos developing over a long period of time, get LVH, get low pressure in aorta, not filing coronaries but have more tissue you need to perfuse.
  38. What is the MOST COMMON CARDIAC VALVE LESION??
    Aortic Stenosis
  39. What is hypertrophic cardiomyopathy?
    Ventricular hypertrophy without an obvious cause such as HTN or AS
  40. What is the prevalence and genetic transmission of hypertrophic cardiomyopathy?
    1 in 500, autosomal dominant
  41. What is the most common cause of SCD (sudden cardiac death) in peds?
    Hypertrophic cardiomyopathy
  42. What are the most common causes of AR as a primary AV leaflet disease?
    rheumatic fever, infective endocarditis, loss of comissural support with cusp collapse, congenital bicuspid AV
  43. What are types of Aortic root disease (causing AR)?
    Degenerative diseases of aorta (Marfans), cystic medial necrosis, dissection, rare conditions
  44. Is there LVH in acute or chronic AR?
    chronic
  45. How do we manage the HD of a patient with aortic regurg?
    • We manage these patients with “fast, full, forward flow”
    • Fast: bradycardia is bad
    • Full: hypovolemia is bad
    • Forward flow: these patients do well w/afterload reduction
  46. What is a main complication of aortic cannulation? How can we help prevent it?
    • aortic dissection
    • We help prevent that by keeping the systolic pressure 90 or less at the time of the Aortic cannulation
  47. How can they tell if there is an impending aortic dissection during cannulation of the aorta?
    • They’re going to have a little pressure sensor on this aortic cannula (it doesn’t go to us, it goes to the perfusionist) but if the perfusionist is reading an aortic pressure of like 20.
    • They’re going to look and what’s the real pressure? Oh the radial mean is 60 and the aortic pressure is 20—then that’s a huge problem and could be an aortic dissection.
  48. What complication can you have during venous cannula placement?
    atrial dysrhythmia is common and it’s not treated because you’re about to go on bypass so when you put that big line in or close to the atria, commonly you’ll see atrial dysrhythmias
  49. What is on the prebypass checklist?
    • Is the anticoagulation adequate?
    • Is the anesthesia adequate?
    • Is the cannulation proper and patent?
    • Turn off infusions.
    • Monitoring in place & checked (pressure transducers, temperature, foley)
    • Inspect pupils (venous congestion = swelling)
  50. What's on the initial CPB checklist?
    • FACE: color, temp, plethora, edema, symmetry
    • EYES: size & symmetry & conjunctiva for chemosis (edema) & injection
    • PUMP LINES: art/venous color difference should be visible
    • ARTERIAL BP: Normally 30-60mmHg
    • PA PRESSURE: <15mmHg
    • CVP: <5mmHg
    • Examine the heart: Distention & contractility
    • Stop ventilation when aortic ejection by the heart ceases
  51. What is the usual origin of Mitral stenosis?
    rheumatic fever
  52. Is mitral stenosis more common in males of females?
    Females  (2:1)
  53. What does the severity of stenosis correlate with???
    Severity of calcification correlates with the transvalvular pressure gradient
  54. In mitral stenosis, what types of conditions may cause the problem to worsen even more?
    volume overload: pregnancy
  55. What is the normal MV area? Mild and severe stenosis parameters?
    • Normal MV area is 4cm2.
    • Mild is 1-2cm2.
    • Severe is less than 1cm2
  56. How do we manage the patient with mitral stenosis?
    • LV filling is important.
    • Important to maintain SR.
    • Avoid tachycardia.
    • Maintain Euvolemia.
  57. What is the problem with acute mitral regurgitation?
    • LA has not undergone adaptive changes that allow for compensation
    • Acute pulmonary edema
  58. Why is LV ejection fraction not a good indicator of LV function in mitral regurgitation?

    What would you measure instead?
    LVEF not good index since LV ejects both into the aorta & LA

    Must measure non-ejection indices of function (LV ESP/LVESV relationships
  59. If there is chronic MR, we wouldn't see pumonary HTN but what would we see?
    atrial fibrillation (stretch of LA)
  60. What 5 things are part of your last minute check before induction?
    • Reassessment of the patient’s overall cardiopulmonary and airway status
    • Integrity of the breathing circuit and suction
    • Availability of blood for transfusion
    • Proximity of a surgeon or fellow
    • Immediate availability of emergency cardiac drugs
  61. Which patients are at high risk for ischemia on induction??
    AS or MS, left main disease, or left main equivalent (it’s a high grade stenosis of both the LAD and circumflex).
  62. What three main things are we concerned about with induction/intubation?
    HR control, coronary perfusion pressure, and O2 supply and demand
  63. We typically give higher doses of Fentanyl on induction for cardiac surgery. Why???
    • Fentanyl is more cardiac stable drug, little effect on contractility and decreases HR.
    • Not complete anesthetic (unless at REALLY HIGH doses)
  64. What can help offset the bradycardia from high dose fentanyl during induction?
    Sometimes if the airway looks normal, pancuronium is used to offset the bradycardia associated w/Fentanyl.
  65. What sedative hypnotics do we use on induction??
    • Etomidate is used frequently, it tends to only slightly (10%) decrease mean pressure so it decreases MAP far less than Propofol.
    • Some people still use Propofol in a much lower dose and we’re watching BP closely on Art line.
  66. What volatile do we avoid in cardiac anesthesia???
    • Nitrous!
    • Because of the bubbles, the blood is going fast to the CPB. There has been some speculation that those little bubbles can cause post-op cognitive dysfunction. Don’t want to expand the bubbles in bypass!
  67. What is the main risk of CVL insertion??
    Main risk of CVL insertion is putting the central line in the carotid artery and not the IJ
  68. When do we extubate the patient in fast track??
    Extubation within 8 hours
  69. Is there an increase in ischemia or resp morbidity and mortality with fast track patients?
    No
  70. How much fentanyl do we give in cardiac anesthesia?
    Lower dose narcotics – Fentanyl limited to 10-15 mcg/kg
  71. Cardiac surgery carries a high risk for intra-op awareness. How can we help prevent this??
    During the procedure, the perfusionist runs Isoflurane. It is a good idea to check w/the perfusionist to make sure it’s on.
  72. Various studies have shown epidural anesthesia may be helpful for fast tracking. What could be an issue w/this?
    Heparinization
  73. What things are we doing pre-bypass (low stimulation time)
    • Want to check pressure points (head and heels well padded, alopecia can happen w/long procedures so pad well and turn slightly.)
    • Ensure all monitors and lines are working.
    • Listen to breath sounds.
    • Drop OG (always oral) and empty the stomach, then the TEE probe is placed. OG so it’s not a distended sack when TEE probe goes down the esophagus.
    • Send baseline labs.
    • Give antibiotics
  74. What baseline labs do we get pre-bypass?
    • Activated clotting time (ACT). 3cc of blood and hand to perfusionist and he runs an ACT.
    • Other labs: BG, electrolytes, glucose is important
  75. When would we need to deepen our anesthetic (Stimulating times) going on bypass?
    • Sternal inscision
    • Sternal split
  76. When do we deflate the lungs going on bypass?
    When the saw is used to open the sternum and the surgeon says lungs down
  77. After the chest is opened, we must switch something....what is it??
    we’re going to switch to internal paddles. Pull out external paddles and then plug in internals. The surgeon will shock from this point on (amp is 10mV)
  78. How much blood should we have available going on bypass?
    She said 2 U of blood immediately available

    If redo heart there could be grafts or the RV actually attached to sternum which could cause a “crash on bypass” because they have adhesions.
  79. What is sympathetic nerve dissection?
    sympathetic nerves are dissected from the aorta to allow for insertion of the aortic cannula. This can be stimulating.
  80. Basically how does heparin work and what is it's 1/2 life?
    • Basically it binds to anti-thrombin III
    • ½ life is 2.5hrs.
  81. What is the normal ACT? What do you need it to be before initiating bypass?
    • Normal ACT is 105-167 seconds.
    • Books say you need an ACT of at least 300sec prior to initiating bypass
  82. When do you draw up protamine?
    Don’t EVER drop up the protamine until you’re off bypass!!! Wait until end of case when you need it.
  83. Why is communication with the surgeon so important when they're lifting the heart?
    The monitors are inaccurate and it's ALWAYS good to communicate
  84. Why is the surgeon concerned w/the TEE before aortic cannulation?
    Sometimes they want to see, are there any calcifications on that Aorta before they cannulate.
  85. On bypass, what should your art line BP read?
    30-60mmHG
  86. Where is cardioplegia usually given?
    • in the aortic root through the aorta.
    • It can be infused retrograde through the coronary sinus.
    • So for example if someone had aortic regurgitation and you couldn’t get the flow back up, you were working on that valve, you could infuse the cardioplegia in a retrograde fashion.
  87. What is cardioplegia?
    • cold high potassium solution that stops the heart
    • varies by institution
  88. How does the surgeon actually do the grafts (which end first)
    First the distal ends  (near the heart) and then rewarming and doing the proximal ends (near the aorta)
  89. The perfusionist will frequently be checking anticoagulation, blood gases, serum electrolytes on bypass. What are we checking for labs?
    Glucose

    You’re checking the blood sugar every 20minutes and the patient’s tend to get hyperglycemic. (d/t cardioplegia solution). Insulin gtts are commonly run by anesthesia
  90. Where do we try to keep the blood glucose level?
    keeping the blood sugar under 150
  91. why would urine output initially be high on bypass?
    some priming solutions have mannitol in it
  92. What could low urine output mean on bypass?
    poor renal perfusion
  93. What are some potential catastrophes of bypass?
    malposition of the aortic cannula, aortic dissection, carotid hypo or hyperperfusion, air block obstructing venous return
  94. What happens as bypass is terminated (Three things listed on denise's slide)
    • Rewarm
    • Remove air if necessary
    • Optimize metabolic condition
  95. What factors make weaning from CPB difficult?
    • fibrillation
    • potassium or acid/base disturbance
    • need for pacing
    • need for inotropic support
    • optimal preload
  96. What cardiac components are on the checklist before seperating from CPB?
    • Surgical (bleeding, valve function, intracardiac air, and aorta-confirm no dissection)
    • Rate and rhythm
    • Ischemia
    • Myocardial function (visual observation, TEE, cardiac output and filing pressures)
  97. when do we start ventilating the patient?
    when the patient is on partial bypass
  98. When can bypass be terminated?
    If you have a systolic BP of at least 90 with a pump flow of 1L or less, bypass is terminated.
  99. What kinds of things can be wrong when terminating bypass?
    • The heart may be need to be defibrillated. This is more likely in valve patients.
    • Pacing may be required.
    • Sometimes it’s a stunned myocardium (not contracting enough) and Ca Cl may be needed (excellent inotrope).
  100. What is "key" in coming off bypass?
    • optimal preload
    • TEE is helpful
    • If on flat portion of starling curve, then inotrope might be needed
  101. When do we give protamine?
    After the venous cannula is removed
  102. How do we give the protamine
    • Pefusionist tells the dose and the surgeon says when to give it
    • Give test dose
    • Give remainder slowly and tell surgeon how much is in as you give it because they're timing when to take out the aortic cannula
  103. We give a test dose of protamine in case the patient has a bad reaction. What kind of reaction may they have and who is most likely to have it??
    Pulmonary HTN & systemic hypotension

    The patient most likely to react to protamine are those on NPH insulin (P is protamine-sensitized to it).
  104. What could cause ischemia and LV failure after CPB?
    graft failure, air in graft, kinking of graft
  105. What could cause inadequate coronary blood flow and LV failure after CPB?
    incomplete revasc (inoperable vessels), inadequate coronary perfusion pressure, emboli, spasm, increased demand
  106. What gas exchange problems might we have after CPB?
    hypoxemia, atelectasis , “pump lung
  107. What is pump lung?
    • Atelectasis is usually mild
    • In it’s most severe state a form of ARDS develops which is called pump lung or post perfusion lung syndrome.
    • Thought to be d/t activated neutrophils in the lung.
    • It is very very rare today because of improved membrane oxygenators in the pump and pump lung is rare
  108. What are the differential diagnosis of LV failure post bypass? (there are six)
    • Ischemia
    • Inadequate coronary perfusion
    • Valve failure
    • Gas exchange problems
    • Preload
    • Reperfusion injury
  109. How do we treat cardiovascular depression?
    INOTROPE: Epi or Milrinone
  110. When is it good to give Epi or Dopamine in cardiac decompensation?
    HR is normal and SVR is low
  111. When is it good to give Dobutamine or Milrinone in cardiac decompensation?
    if SVR is increased
  112. What should you give if HR is elevated in cardiovascular decompensation?
    Milrinone or Low dose Epi
  113. What types of patients are at risk for RV failure?
    • pulm hypertension
    • mitral valve disease
    • RV infarct or ischemia
    • RV outflow obstruction
    • tricuspid regurg
  114. How would you treat RV failure?
    • NTG if systemic BP permits
    • optimize preload
    • preserve coronary perfusion pressure
    • inotropic support – Milronone, Dobutamine
  115. TRUE or FALSE. Protracted RV failure carries a very poor prognosis.
    TRUE
  116. We want to hyperventilate to lower PVR in RV failure but more than anything we want to prevent increased PVR. How do we do this?
    Avoid hypoxemia, acidosis, and nitrous oxide
  117. Coming off bypass we make sure the temperature is 37. Why does it drop post CPB?
    After drop in temperature, initially coming off you get all the way up to 37 and then it will slowly fall off again. During initial rewarming, some peripheral vascular beds do not dilate and so they act as a reservoir for cold blood.
  118. What are some complications of transferring a cardiac surgery patient to the ICU?
    • extubation
    • coronary or air embolism from dislodgement
    • invasive line removal
    • IABP line disruption
    • pacemaker wire disconnect
    • corneal injury
    • loss of vasoactive infusions
    • venodilation and hypotension
  119. What are some advantages of off pump CAB?
    • Avoidance of CPB
    • Less risk of stroke or neuropsychiatric deficits
    • shorter hospitalization and ICU stay
    • Lower cost
    • Lower tranfusion requirement
  120. What are some disadvantages of off pump CAB?
    • Technically more demanding
    • Multivessel disease is contraindicated
    • May not be a reproducible technique
    • HD instability and arrhythmias
    • Unsafe in unstable patients
  121. What are the unknowns about off pump CAB?
    • Operative risk
    • Appropriate patient selection
    • Short and long term graft patency rates
    • Adequacy of overall revascularization
    • Cost considerations

Card Set Information

Author:
 cmatthews
ID:
 260010
Filename:
 Cardiac Adv. Principles
Updated:
2014-02-04 02:31:33
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BC CRNA Cardiac Surgery
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From Denise's online principles class
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