Cardiac- Coexisting review 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
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
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
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
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!
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
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
- unstable CAD (major clinical risk factors and/or change in cardiac condition
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
- < 5 yr, no change in medical condition
- PCI
- BMS > 6 wk- minimal antiplatleet therapy; no change
- no need stress test, proceed to sx
- BMS > 6 wk- minimal antiplatleet therapy; no change
- DES <12 MO AND dual antiplt therapy
- consult cardiology to blaance risk of thrombosis and/or bleeding
- cabg
- If no prior revascularization
- statify risk further (see next slide)
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
- noninvasive testin (stress test)
- stable CAD (medically optimized or good exercise tolerance)
- If cath shows left mian or equivalent disease–> multidisciplinary approach
- consider risk of noncardiac sx vs coronary revascularization
Refresh high/intermediate risk sx
- high risk
- aortic
- major vascular sx
- peripheral vascular sx
- intermediate
- intraperitoneal/intrathoracic
- CEA
- Head/neck sx
- orthopedic
- prostate
- low
- endoscopic
- superficial
- cataract
- breast
- ambulatory
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!
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
-
II, V5 give idea of inferior and anterolateral aspect of heart
- If specific area has hx ichemia, then minotr that area (ie, circumflex, monitoring I, avL)
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
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,
- MVO2- controlling demand is easier than supply, attenuate sympathetic outflow
- focus on controlling (decreasing) DEMAND in CAD pt
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
- hypercoaguable state, plaque rutpures–> thrombus /embolus
- 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!
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
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 hoursdon’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
- SNP 0.5-10 ug/kg/min
-
Meds:
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?
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
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
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
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
21
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
22
Q
Monitoring of HTN pt?
A
- 5 lead EKG
- A line, CVP, PA cath if extensive sx and venricular dysfunction
- TEE
23
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
24
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
- if yes, then HTN treat with
25
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
26
Q
Preferred anesthesia technique for PAD pt?
A
- Regional anesthesia: some perceived advantages of regional anesthesia
- increased graft blood flow
- sympathectectomy below level of regional
- less increase in SVR with cross clamping
- Postop pain relief- this also protects SNS outflow
- Less activation of coag system
- decrease plt activation
- decrease resistance in blood flow
- preferrable mechanism- consider anticoag/antiplt meds pt on!
- increased graft blood flow
-
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
27
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
28
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
29
Q
Goal of managmenet of mitral stenosis pt?
A
Goals (slow tight full)
- Avoid sinus tachycardia or rapid ventiruclar response rate during a fib
- Stoelting- treat afib c rvr with amiodarone, bb, ccb
- 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!
- avoid drug induced decreases in SVR
- use etomidate- any decrease in SVR, hypotension is very difficult to manage, need to treat adequately with phenylephrine
- 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
30
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
31
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
32
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
33
Q
Aortic stenosis general management goals of anesthesia?
A
- Important goal– avoid events that would further decrease CO
Goals (slow, tight, full like MS??)
- maintain NSR
- AVOID bradycardia or tachycardia
- hr 60-90 hr DEPENDENT on BP
- avoid hypotension
- If lose BP, like MS, will get into trouble
- 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!
34
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)
35
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
- Avoid sudden decrease in HR
- HR 80/85 beneficial
- Avoid sudden increase in SVR
- need good forward flow
- if you decrease BP, hard time getting them back
- also avoid sudden increases
- Monitor the size of the V wave as a reflection of regurgitant flow
- minimize drug induced myocardial depression
- want balanced technique, with opioid, some VA, nsaids, tyneol etc.
- no high VA
36
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
37
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
- If LV dysfunction not severe:
- Use of invasive monitorign- depends on:
- compelxity of procedure
- magnitude of physiologic impairment with MR
38
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
39
Q
Induction of anesthesia with aortic regurg?
A
- Use drugs considered likely to maintain forward LV stroke volume
- etomidate- cardiac stable
40
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
41
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
42
Q
Goal of anesthetic managmenet in patient with HF?
A
Goal is to prevent and avoid myocardial depression
- HR- normal to elevated
- Preload- normal to high!
- if drop preload, then low SV
- 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
- Contractility- increase
43
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
44
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
