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CO-EXIST Test 4! > Cardiac > Flashcards

Cardiac Flashcards

1
Q

Pharmacologic Management for CAD pts? Anesthesia implications of normal pharmacologic mgmt?

A

Get good H&P- confirm current med management

  • Beta blockers
    • reduce contractility and HR
    • Make sure they’re still taking
  • CCB
    • dilate coronary arteries
    • reduce contractiliy
    • reduce afterload
  • ACE inhibitors
    • imporve contractility by afterload reduction
    • 1st line for HTN and DM
    • Can cause intraop HoTN- d/c 24 hours before
  • Nitrates-
    • dilate coronary arteries and collateral blood vessels
    • decrease peripheral vascular resistance (decreases afterload)
    • vendodilation (decreases preload)
  • Antiplt drug
    • reduce potential for thrombosis
    • consider INR and ability to perform regional
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2
Q

Periop MI risk?

A
  • Risk of periop death d/t cardiac cause is <1% ingeneral population
  • Most periop MIs occurs in frst 24-48 hours after surgery
    • d/t pain, stress, no anesthesia
    • don’t set them up for failure- use appropriate adjuncts
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3
Q

What time shoudl you wait for elective surgery after angioplasty without stent, BMS placement, CABG, Drug-eleuting stent placement?

A
  • Angioplasty without stenting- 2-4 weeks wait
  • Bare metal stent placement- wait at least 30 days; 12 weeks preferred!
    • 3 months ideal
  • CABG- wait 6 weeks; 12 weeks preferred
    • frequently CABG done before elective sx
  • Drug eluting stent placement - at least 12 months
    • drug eluting stnet has antineoplastic/abx coverage that dissolves in few weeks–> month, prevent rethrombose/PLT aggregation
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4
Q

What causes decreased O2 supply?

A
  • Tachycardia (decrase diastolic time)
    • treat underlying cause to treat tachycardia! (pain, hypovolemic, anemic, etc)
  • hypotension- decrease perfusion pressure to heart
  • vasoconstriciton- avoid phenylephrine
  • O2 carrying capacity
    • acid/base
    • anemia- replace blood with blood!
    • hypoxia FIO2 >70%
  • Viscosity- dry, more resistance in vessel, decrease supply
  • Arterial patency- can’t control, underlying condition
  • coronary spasm- avoid by reducing stress by preemptic analgesia
    • esp in areas with atherosclerosis. avoid drugs that cause coronary spasm and use drugs like CCB to help increase supply by reducing vasospasm
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5
Q

What are factors that increase O2 demand to heart?

A
  • Tachycardia (this one is also on decreased supply list)
  • Increase Contractiilty- b blockers
  • increased preload- normal volemic patient
  • increased afterlaod
  • shivering- increase metabolic demand
    • keep pt warm
  • hyperglycemia- tight control
    • manage SNS to prevent hyperglycemia
  • HTN- d/t pain
    • treat pain! manage BP!
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6
Q

Goal of managing O2 supply and demand to heart?

A

Prevent tachycardia and treat immediately because it’s the only one that affects both supply and demand negatively

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7
Q

What is first step to decide if CAD pt can proceed to sx?

A
  • Determine if emergent or urgent:
    • optimiize medical management/proceed to surgery
  • If Elective:
    • unstable CAD (major clinical risk factors and/or change in cardiac condition
      • cardiology consultation
    • Stable - next slide
      • determine exercise tolerance, see next slide for further info
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8
Q

Pt with stable CAD is having elective sx, what are steps to determine if further testing necessary?

A
  • Determine exercise tolerance
  • High or intermed risk sx and moderate to minor clinical risk factors
  • if prior revascularization
    • cabg
      • < 5 yr, no change in medical condition
        • no need for stress test, proceed to sx
    • PCI
      • BMS > 6 wk- minimal antiplatleet therapy; no change
        • no need stress test, proceed to sx
    • DES <12 MO AND dual antiplt therapy
      • consult cardiology to blaance risk of thrombosis and/or bleeding
  • If no prior revascularization
    • statify risk further (see next slide)
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9
Q

How do you determine If stable CAD with no prior revascularization can proceed to sx?

A
  • If high or intermediate risk sx or moderate clinical risk factors with no prior revascularization
    • stable CAD (medically optimized or good exercise tolerance)
      • no need to stress test
      • proceed to sx
    • unable to assess CAD or decreased exercside tolerance
      • noninvasive testin (stress test)
        • if positive–> cardiac cath
        • if negative–> proceed to sx
  • If cath shows left mian or equivalent disease–> multidisciplinary approach
    • consider risk of noncardiac sx vs coronary revascularization
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10
Q

Anesthetic mgmt for pt with CAD?

A
  • Regional
    • tx hypotension with phenylephrine- okay for short periods
    • if bradycardic- use ephedrine
  • General
    • maintain blanace b/w supply and demand
    • do not allow for long periods of hypotention
    • Wake up warm, don’t overload with fluids, don’t admin too much phenyl and cause increase afterload
  • IMPORTANT TO MAINTAIN BP WITHIN 20% OF PT BASELINE!
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11
Q

How do you appropraitely monitor for ischemia in sx?

A
  • EKG 5- lead at least for angina
  • See table for leads, coronary artery responsible and area of myocardium involved. probably wise to memorzie for test ;-)
  • Dr. E mentioned II. III, V5 being most ideal to monitor for ischemia; these are the areas with increased likelihood for ischemia
    • ​II, V5 give idea of inferior and anterolateral aspect of heart
      • ​that side is more muscular, in diastole, doesn’t fill as proficiently
  • If specific area has hx ichemia, then minotr that area (ie, circumflex, monitoring I, avL)
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12
Q

Induction of patient with CAD?

A
  • minimal hemodynamic effect (no wide swings in BP!)
    • keep duraiton of laryngoscopy short!
    • minimize response
      • opioids upfront
      • LTA, IV lidocaine, before DL
      • Be efficient, no significant changes to your technique
      • deep, smooth induction
  • Severe cardiac dysfunction
    • etomidate
    • high opioid technique
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13
Q

Anesthesia maintenance of pt with CAD?

A
  • AVOID TACHYCARDIAS!
  • Preload- normal
  • afterload- normal
  • contractility- decrease if LVF is normal- if LVF is reduced, don’t mess with it
    • continue BB unless LVF decrease
  • HR- avoid increases
  • Rhythm- NSR is best,<– rely on atiral kick
  • MVO2- controlling demand is easier than supply, attenuate sympathetic outflow
    • focus on controlling (decreasing) DEMAND in CAD pt
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14
Q

Intraoperative considerations for CAD pt?

A

All patients undergoing sx will have normal inflammatory response and neuroendocrine stress response. Focus on managing effects of these responses:

  • Inflammatory response
    • hypercoaguable state, plaque rutpures–> thrombus /embolus
      • decreased HCT, hypoxia, vasoconstriciton, decreased BP all contribute to decreased O2 delivery
  • Neuroendocrine response
    • Increase HR increase BP, metabolic changes
    • postop shivering
    • all cause increase O2 demand
  • Decreased O2 delivery and increased O2 demand–> perioperative myocardial injury/infarction which can show up 1-2 days postop!!

To minimzie response intraop:

  • Smooth anesthetic
    • No big fluctuates in HR/BP
    • Admin
      • Opioids
      • intraop tylenol
      • toradol
      • steroids
  • Wake up pain free
  • keep pt warm
  • address blood loss
  • keep well oxygenated!
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15
Q

What is definition of hypertensive crisis? Treatment?

A

Definition: sudden increase in diastolic BP above 130 mmHg

  • due to: activation of RAAS system<– usually what sets off crisis

TREATMENT:

  • Prompt, but controlled reduction in BP with NTP (SNP) 0.5-10 ug/kg/min
  • Monitoring UOP (foley) and insertion of intraarterial BP
  • Decrease DBP carefully to 100-110 mmHg over several min to hours<– don’t want to drop too quick!
    • ​Meds:
      • SNP 0.5-10 ug/kg/min
        • DOC, short DOA
      • NTG 5-200 mcg/min
      • Labetalol 40-80 mg q 10 min
        • careful, don’t want to BB heart!! use with arterial dilator like SNP!!
      • Esmolol 50-300 MCG/KG/MIN
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16
Q

Quesitons to consider for anesthetic managmenet of HTN patient?

A
  • Controlle vs uncontrolled HTN?
  • Emergent vs elective sx?
  • Evidence of end-organ damage?
    • angina
    • CHF- problematic d/t increased M/M r/t recent CHF exacerbation
    • CVA- how long ago? what weakness, mentla status?
    • Renal insufficiency- HTN often has renal insuff. Do you expect big fluid volume shifts intraop? may want foley/aline
    • PVD
  • Drug regmien?
    • BB? ACE? ARB? CCB? Did they take them?
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17
Q

Management of anesthesia for HTN pt?

A
  • Preop eval
    • determine adequacy of systemic BP control
    • review pharmacology of drugs being admin to control systemic BP (orthostatic hypotension, bradyacrdia, sedation_
    • Evaluate for evidence End organ damage
      • angina
      • LVH
      • CHF
      • CVA
      • PVD
      • Renal insufficiency
  • Induction
    • anticipate exaggerated systemic BP
    • Limit duraiton DL to avoid HTN
  • Maintenance anesthesia
    • admin VA to blune HTn response
    • monitor for MI
  • Post op
    • anticipate periods of systemic HTN
    • maintain monitoring of end organ function
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18
Q

Induction goals for HTN patient?

A
  • Goal is to minimize SNS stimulationw ith laryngoscopy and intubation
  • attenuate laryngeal reflexes with additional narcotic, increase VA, and lidocine (topical or IV)
  • How?
    • choice of any induction agent is appropriate EXCEPT ketamine (Increase SNS resposne)
    • Lidocaine IV 1-1.5 mg/kg
    • Lidocaine Topical LTA 2-4%
    • opiates
    • VA
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19
Q

Maintenance goals in patient with HTN?

A
  • Goal is to adjust depth of anesthesia to minimize wide shifts in hemodyanmics
    • drop Bp right before DL because it will get dramatically high with DL
  • Be prepared for wide shifts- typical with HTN patients
  • How?
    • Choose IA that is easily adjusted (des, sev)
    • Balanced technique
    • have ephedrine, neosynephrine readily available
    • consider neo gtt if unable to get adequate depth of anesthesia
      • used to living at higher perfusion pressure, keep BP within 20%!!
20
Q

Postop consideration for pt with HTN?

A
  • Goal is to minimize SNS secondary to srugical pain and n/v
  • no shivering!!
21
Q

Intraop HTN treatment?

A
  • Usually d/t pain!
  • incidence is higher in pt with essential HTN
  • treatment:
    • narcotics- if pain is obvious cause
    • IA
    • BB
    • NTG
    • Nipride
22
Q

Treatment of intraop hypotension?

A
  • Decrease aneshtesia depth
  • fluids
  • sympathomimetics
  • check rhythm–> is it junctional? sometimes pt go into junctional rhythm under anesthesia, unsure exact mechanism
    • maintain normocapnia
    • avoid high concentration of IAs
23
Q

Monitoring of HTN pt?

A
  • 5 lead EKG
  • A line, CVP, PA cath if extensive sx and venricular dysfunction
  • TEE
24
Q

Emergence of pt with HTN?

A
  • Controlle emergence
  • minimize sympathetic outflow- every HTN pt will wake up HTN
    • use of narcotics
    • use of lidocaine
    • use of labetalol, esmolol, NTG
    • Deep extubation- if possible
25
Q

Post op HTN treatment?

A
  • Pain adeuqately controllw?
    • if yes, then HTN treat with
      • hydralazine 2.5-10 mg IV q 10-20 min
      • labetalol 5-20 mg IV q 10 min
      • Nipride 0.5-10 mcg/kg/min
26
Q

Peripheral revascularization for peripheral vascular disease (PVD)

A
  • Preop:
    • Assess HTN and CAD r/f for PAD
    • Exercise tolearance, pain, claudication with exercise? blood thinners?
  • Intraop:
    • After donor and recipient arteries exposed, tunnel is created and graft is passed
    • graft may be saphenous vein or prothesis
      • own vessel doesn’t work that well because probably also atherosclerosed
    • Heparin IV given
      • typically give 3,000-5,000 units
    • Anastomosis are constructed
    • arteriogram to confirm adequate flow- doppler peripherally to confirm adequate flow
      • ​maintain good BP in these pts!
    • heparin is not likely to be reversed
  • Principle risk during reoncstructive sx is associated with atherosclerosis, especially IHD
    • Pt with PVD has 3-5greater risk of MI, stroke and death!
    • need good exercise tolerance! cleared by cards, stress test, etc
    • have to manage both PVD and CAD!
  • CABG operations are usually performed before sx on peripheral vasculature pt who experience angina and claudication
27
Q

What is important in management of PVD pt?

A

skill and experience of anesthesia provider, including the ability to monitor hemodynamics and respond quickly, are far more important than a specific agent used

28
Q

Preferred anesthesia technique for PAD pt?

A
  • Regional anesthesia: some perceived advantages of regional anesthesia
    1. increased graft blood flow
      • sympathectectomy below level of regional
    2. less increase in SVR with cross clamping
    3. Postop pain relief- this also protects SNS outflow
    4. Less activation of coag system
      • decrease plt activation
      • decrease resistance in blood flow
      • preferrable mechanism- consider anticoag/antiplt meds pt on!
  • Regional vs General
    • assess for coag
    • if consideration regional, spinal may be best, to avoid hematoma
    • studies have shown no diff b/w RA and GA in terms of CARDIOPULMONARY complications
      • no diff in MI, death, myocardial ischemia outcomes b/w regional and GA
    • sig difference in complication rate in terms of GRAFT OCCLUSION
      • pt c reigonal do better with graft and graft sx outcome
      • surgeons want regional
29
Q

Anesthetic management of PAD?

A
  • Consider co morbiidties- biggest CAD
    • CVA, renal, etc?
  • medication hx- impact on anesthetic delivery
    • anticoag–> if increased INR, no regional
  • end organ perfusion and oxygenation– maintain
    • kidney, brain
  • blood gases- electolyte and pH changes
  • cross clamp- hep admin/record time/reversal?
    • give heparin (3-5000 max)
    • record time–> heparin peaks 3-5 min after, let surgeon know and they’ll cross clamp
    • typically no reversal needed unless higher doses given
30
Q

Peripheral revascularization monitoring?

A
  • Pt typically present with CAD, DM, HTN
    • tight BG control
  • Preop- make sure pt takes BB and/or other chronic meds
  • intraop a line- useful if labile BP and bypassing large vessels, long case
  • ability to monitor intravascular volume by either CVP and CO or urinary catheter
    • esp is underlying cardiac issues
    • foley with longer cases esp.
  • EBL- keep eye on blood loss. if not clamping adequately, may get quite a bit of bleeding
  • estimated third space
    • wounds can be large OR sometimes small incisions
    • keep eye on third spacing
31
Q

Goal of managmenet of mitral stenosis pt?

A

Goals (slow tight full)

  1. Avoid sinus tachycardia or rapid ventiruclar response rate during a fib
    • Stoelting- treat afib c rvr with amiodarone, bb, ccb
  2. avoid marked increases in central blood bolume as associated with over transfusion or head-down position
    • no rapid transfuion or head down
    • dont’ want drop or sudden increase in prelaod!
  3. avoid drug induced decreases in SVR
    • use etomidate- any decrease in SVR, hypotension is very difficult to manage, need to treat adequately with phenylephrine
  4. Avoid events such as arterial hypoxemia and/or hypoventilation that may exacerbate pulmonary HTN and evoke RV failure
    • ​will easily back up into pulmonary system!
    • 100% o2 prudent on these pt
    • Stoelting- events that increae pulm HTN=
      • ​Hypoxemia
      • hypercarbia
      • lung hyperinflation
      • increase lung water
32
Q

Induction of anesthesia in pt with Mitral stenosis?

A
  • Most often accomplished with drugs admin intravenously that are unlikely to increase HR (avoid ketamine) or abruptly decrease SVR (want to maintain tight system)
    • ​ideal- etomidate, high narcotic technique
33
Q

Maintenance of anesthesia with mitral stenosis?

A
  • Is intended to minimize the likelihood of marked and sustained changes in HR, SVR, PVR and myocardial contractility
  • useful drugs
    • beta blockers
    • ccb
    • phenylephrine
  • Use of invasive monitoring depends on complexity of the operative procedure and the magnitude of physiologic impairment produced by mitral stenosis
    • aline useful—-degree of invasive monitoring depends on procedure and sx impairment
    • if very severe MS and non-cardiac related procedure, is the procedure worth doing before valvular replacement?
    • If sx needs to be done and MS isn’t so severe
      • ​aline
      • CVP line useful
    • if bigger procedure–> cardiac consult esp if mitral stenosis severe
34
Q

What intraop events do you need to avoid with MS?

A
  • Sinus tachycardia or rapid ventricular response during atrial fib
    • BP will instantly drop
  • marked increase in central blood volume, as associated with overtransfusion or head down positon
  • drug-induced decrease in SVR
    • If Bp drops, hard to get blood flow back
  • hypoxemia and hypercarbia that may exacerbate pulmonary HTN and evoke RV failure
35
Q

Aortic stenosis general management goals of anesthesia?

A
  • Important goal– avoid events that would further decrease CO

Goals (slow, tight, full like MS??)

  1. maintain NSR
  2. AVOID bradycardia or tachycardia
    • hr 60-90 hr DEPENDENT on BP
  3. avoid hypotension
    • If lose BP, like MS, will get into trouble
  4. optimize intravascular fluid volume to maintain venous return and LV filling
    • ​need good venous return! help with SV and forward flow
    • don’t overload either!
36
Q

Gen vs regional in aortic stenosis?

A
  • General anesthesia is often selected in preference to epidural or spinla anesthesia
    • this minimies the likelihood of an undesirable decrease in SVR
    • sympathemectomy with spinal causes lots of issues with AS!
  • Use of a-line and PA catheter depends on magnitude of sx and the severeity of the aortic stenosis
    • BIG procedure, severe AS and can’t replace before urgent/emergent sx, make sure you have PA, a line and moniroting (TEE may also be useful)
37
Q

Goal of management of anesthesia with Mitral regurgitation?

A
  • Important goal is to avoid events that may further decrease CO

GOAL : FAST FULL FORWARD

  1. Avoid sudden decrease in HR
    • HR 80/85 beneficial
  2. Avoid sudden increase in SVR
    • need good forward flow
    • if you decrease BP, hard time getting them back
    • also avoid sudden increases
  3. Monitor the size of the V wave as a reflection of regurgitant flow
  4. minimize drug induced myocardial depression
    • want balanced technique, with opioid, some VA, nsaids, tyneol etc.
    • no high VA
38
Q

Induction of anesthesia in mitral regurgitation?

A

Keep in mind the importance of avoiding excessive and abrupt changes in SVR or decrease in HR

  • Keep those things in mind when choosing drugs
  • Etomidate is best bet- no change in BP/HR
39
Q

Maintenance of anesthesia with mitral regurg?

A
  • Maintenance of aneshtesia- is influenced by degree of LV dysfunction
    • If LV dysfunction not severe:
      • N2O plus VA (isoflurance is attractive choice because of hemodynamic effect)
    • LV dysfunction severe:
      • use of opioid technique- minimizes likelihood of drug-induced myocardial depression, may be a consideration
  • Use of invasive monitorign- depends on:
    • compelxity of procedure
    • magnitude of physiologic impairment with MR
40
Q

Anesthetic management of aortic regurgitation?

A

Goals:

  • avoid sudden decrease in HR (high normal)
  • avoid sudden increase in SVR - blood will go back
  • minimize drug induced myocardial depression
41
Q

Induction of anesthesia with aortic regurg?

A
  • Use drugs considered likely to maintain forward LV stroke volume
    • etomidate- cardiac stable
42
Q

Maintenance of anesthesia with aortic regurg?

A
  • If no severe LV dysfucntion
    • N2O plus VA (isoflurane attractive choice d/t minimla hemodynamic effects)
  • When myocardial function compromised
    • use of opioid alone may be considered
43
Q

In a pt with aortic regurg, how aggressively should replace fluids?

What physiologic state requires prompt treatment?

What determines the monitoring needed in an aortic regurg patient?

A
  • Prompt replacement of blood loss important to maintain forward LV stroke volume
    • if losing blood, repalce blood!
  • bradycardia may require prompt treatment with atropine (or glyco)
  • Monitoring is dictated by
    • complexity of sx
    • severeity of aortic regurg
44
Q

Goal of anesthetic managmenet in patient with HF?

A

Goal is to prevent and avoid myocardial depression

  1. HR- normal to elevated
  2. Preload- normal to high!
    • ​if drop preload, then low SV
  3. Afterload- low
    • ​don’t want open-wide system, if drop BP too much, hard time getting back
    • also want to decrease afterload to decrease workload on heart
  4. Contractility- increase
45
Q

Anesthetic management HF?

A
  • Maintain med therapy- esp BB
  • Hypotension treated with:
    • ephedrine
    • phenylephrine
    • vasopressin
  • GA doses may be decreased (VA, induction)
  • PPV beneficial in decreasing pulmonary congestion
  • regional anesthesia ok
    • if regional and decrease in afterload, be careful because if BP dropped too much, hard time getting it back up
  • Avoid fluid overload
  • +/- arterial line
    • depends on severity of dx and procedure
46
Q

Anesthetic management in IHHS?

A
  • VA good - decrease contractility
    • ​these hearts are too muscular and VA is helpful in decreasing contractility
  • A-line MUST HAVE
  • Treat hypotension with alpha adrenergic agonists (phenylephrine) and VOLUME!
  • Beta adrenergic agonists are contraindicated
    • ​If hypotensive, avoid beta agonists because if they are hypotensive, they’re usually hypovolemic!!! Beta agonists will just make hypertrophy worse!!
  • prompt replacement of blood and fluids
  • avoid vasodilators
  • maintain NSR

CO-EXIST Test 4! (6 decks)

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