Cardiac Flashcards

1
Q

Standard way to eval for cardiac risk?

A

Want to follow AHA/ACC 2014 guidelines:
1) Do thorough H&P (angina, SOB, peripheral edema/elevated JVP)
2) Assess pt’s risk of undergoing a MACE (major adverse cardiac event) using RCRI
3) If elevated, determine METS. If low or N/A, determine with surgeon if possibility of intervention to optimize or not (CABG, PCI, or surgeon’s willingness to operate?)
4) If results of stress test would alter management, order it

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2
Q

RCRI factors (6) and how many in order to be considered to have an elevated risk for MACE?

A

1) Insulin dep DM
2) Hx of ischemic heart disease
3) Hx of compensated/prior HF
4) Hx of cerebral vascular disease
5) Renal insufficiency
6) Intra-peritoneal, intra-thoracic, or suprainguinal vascular surgery

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3
Q

During a code, what are some things you can evaluate for using echo?

A
  • Assess for any RWMAs
  • PE
  • cardiac tamponade
  • HF (R and L heart contractility)
  • Acute dissecting aneurysm
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4
Q

Two types of pharmacological stress tests?

A
  • Dobutamine stress test
  • Adenosine Thallium stress test
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5
Q

Good way of explaining why regional anesthesia is good for pt w/cardiac disease?

A
  • better HD stability
  • avoid myocardial depression ass w/GA
  • avoid need for tracheal intubation + associated symp response
  • reduce need for vasopressor administration w/associated inc in afterload
  • continues neuro assessment of pt since awake (important in certain cases, like CEA)
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6
Q

Good way of explaining what preop anxiety can lead to (detrimental effects on heart)

A
  • inc in HR, SVR, and myocardial O2 consumption
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7
Q

What is myocardial preconditioning?

A
  • exposure to certain drugs protects myocardium against subsequent myocardial ischemia and reperfusion injury (mech not well defined, prob d/t their dose-dep dec in myocardial contractility and loading conditions)
  • 0.25 MAC volatile (iso, sevo, des all w/similar efficacy) may limit infarct size, prevent dysrhythmias, preserve myocardial fxn
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8
Q

What to do if your pt starts developing ST dep?

A

Attempt to optimize myocardial O2 supply/demand by:
- ventilating w/100% FiO2
- correcting any anemia
- treating tachycardia
- possibly dec afterload (carefully, since dec SVR risks cerebral perfusion): NTG has short DOA and benefits on coronary circulation

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9
Q

How to answer:
“Patient’s blood pressure decreases to ___ (82/60 or whatever) - what do you do?

A

1) recheck BP
2) ensure adequate ventilation/oxygenation
3) look at the EKG for signs of ischemia or arrhythmia
4) look at surgical field for excessive bleeding
5) place in Tburg
6) give fluid bolus
7) consider vasoconstrictor administration

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10
Q

Two p waves for every QRS in pt w/previous heart transplant - what’s going on?

A

Unlikely to be heart block, instead likely native atrial tissue (sinus node) creating an impulse that is not conducted over the anastomotic line

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11
Q

Would you perform a neuraxial technique for TKA in pt with transplanted heart? Why/why not?

A
  • Wouldn’t do a spinal bc rapid drop in preload and heart can’t compensate with inc HR
  • Would do a slow epidural instead if issues with doing a GA (difficult airway, etc)
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12
Q

Any differences in monitors for a GA in pt w/previous heart transplant undergoing noncardiac surgery?

A
  • art line
  • +/- central line (d/t reliance on preload rather than HR, better able to assess fluid status)
  • foley (again, fluid status)
  • peripheral nerve monitor since immunosuppressant meds can affect NMB
  • immunosuppressants inc infx risk, so strict aseptic techniques for all invasive monitor placement
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13
Q

Explain induction for pt w/hx of severe asthma, MP III, and heart transplant

A
  • B2 agonist
  • difficult airway equipment available
  • isoproterenol available (direct beta to inc HR PRN)
  • ketamine and inhalational induction
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14
Q

Would you administer glycopyrrolate when giving neostigmine to a heart transplant patient to reverse them?

A
  • yes, because these pts have been shown to recover some of their parasymp innervation back 6 mo post tx, so don’t want to risk it
  • also want to counteract the noncardiac effects of a cholinesterase inhibitors agent like neostigmine (salivation, bronchospasm)
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15
Q

Other possible organ issues 2/2 hx of cardiac transplant?

A
  • renal dysfxn 2/2 cyclosporine
  • gastritis 2/2 chronic steroids
  • immunosuppression and infx
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16
Q

Risk factors for late stent thrombosis s/p DES?

A
  • cessation of DAPT!! #1 most significant factor (should wait 6 mo)
  • multiple, small vessel, bifurcation, and ostial lesions
  • long or overlapping or malappositioned stents
  • dec LVEF
  • hypercoag states (preg, malignancy, DM)
  • DM
  • renal insuff
  • major cardiac events w/in 30d of PCI
  • operation (inc catecholamines, inc pltl aggregability, dec fibrinolysis)
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17
Q

How long before proceeding with elective surgery s/p DES? BMS?

A

DES:
- 6 mo for completely elective
- 3 mo (w/newer generation DESs) if delay of surgery risk > expected risk of stent thrombosis
- if do continue w/surgery w/in these time frames, should continue DAPT, monitor for signs of stent thrombosis, and confirm availability of interventional cardiologist

BMS:
- 1 mo for elective

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18
Q

How is “bridging tx” is employed in a situation where the bleeding risk is too high if DAPT is continued?

A
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19
Q

What to do if have persistent PVCs?

A
  • how frequent? >3/min, polymorphic, runs of >2, R-on-T = inc rate of VT/VF
  • ID any hypoxemia, MI, hypoK, hypoMg, irritation from CVC/PAC
  • d/c any pro-dysrhythmic/QT prolonging drugs
  • get defib in room
  • if became unstable: overdrive pacing or meds (amio, procainamide, BB, sotalol)
  • if VT: stable (amio), unstable (shock)
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20
Q

Ddx for hypoTN (trauma)

A
  • spinal shock (loss of cardioaccelerator fibers T1-T4)
  • anesthetic OD
  • PE (long bone fx, etc)
  • PTX (rib fxs, CVC)
  • cardiac tamponade
  • occult bleeding (abd, thorax, long bone fx)
  • blunting of RAS system by lisinopril
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21
Q

In pt w/WPW and asthma, do you admin B agonist?

A
  • No, bc at risk for re-entrant tachy, pre-excited afib, vfib
  • Obviously at inc risk of hypoxia and bronchospasm, so have B agonist and epi readily available to be able to admin if absolutely necessary
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22
Q

What to do and administer to patient w/asthma and WPW who develops narrow complex tachy?

A
  • likely re-entrant tachy (SVT)
  • wouldn’t choose BB here d/t asthma
  • have surgeon stop stimulation
  • give 100% FiO2 and call for EKG
  • apply patches for cardioversion in case pt becomes HD unstable
  • give 6mg adenosine to slow AV nodal conduction, consider CCB or amio
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23
Q

What is the periop d/c of BB associated with? What about starting BB if not already taking any?

A

Inc risk of MI and chest pain
ACC/AHA guidelines: class I rec to continue BB if already taking them

High-dose, untitrated BB is a/w/ inc incidence of hypoTN, brady, stroke, overall mortality. Best to initiate 2-7d prior to surgery and titrate to HR 60-80

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24
Q

For thoracic aneurysm repair, what is the point of the lumbar drain?

A
  • would allow for passive drainage of CSF to allow for better preservation of spinal cord perfusion. PP = distal aortic P - CSF (or CVP, whichever is highest)
  • spinal cord usually controlled by autoreg, but this can be impaired, + clamp induced increases in CSF P —> careful drainage is reasonable strategy
  • be careful if they’re on anticoagulation/antipltlts! D/c for however long before and after insertion/removal
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25
Q

What is a word for the antiplatelets like clopidogrel, prasugrel, ticlopidine, etc?

A

Thienopyridines

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26
Q

What are the ASRA guidelines for neuraxial procedure if patient is on heparin and GP IIb/IIIa inhibitor? How long to wait for each

A
  • platelet aggregation normalizes following d/c of GP IIb/IIIa in 4-8 hrs, and 4-6 hours after IV heparin. So wait 8 hrs before placement
  • GP IIb/IIIa inhibitors used for bridging tx when pt who requires thienopyridine tx (clopidogrel, etc) to prevent stent thrombosis must undergo surgical procedure where risk of bleeding makes continuation of long acting platelet inhibitor unacceptable
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27
Q

How do you manage epidural placement/removal if have to go onto CBP? Like in thoracic aneurysm repair etc

A
  • ensure preop anticoags stopped for appropriate length of time (e.g. 8 hours for GP II/III inhibitors, heparin IV)
  • delay systemic heparinization for 60min after epidural placement
  • use smallest amount of heparin necessary
  • monitor carefully for s/s of epidural hematoma
  • ensure adequate coagulation at time of catheter removal
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28
Q

Details about the art line for thoracic aneurysm repair?

A
  • Need two: one in UE, one in LE (will be doing partial bypass on lower body, remember convo w/C, you’ll essentially need to maintain the correct MAP through the bypass circuit so as to not steal too much flow from the upper body and not allow the native heart to pump adequately
  • In their answer, they say to have the UE one on the R arm since clamping of the L subclavian might be necessary (if aneurysm involves proximal descending aorta, clamp may be placed proximally)
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29
Q

Why place a PAC in a particular case? Benefits to it

A
  • fluid management
  • assessment of cardiac fxn
  • timely ID of cardiac ischemia intraop
  • TEE would also help with all of these things, but is not continued postop so is best to work with both intraop for comparison purposes in order to feel more comfy relying on data from only PAC afterwards
  • e.g. could have inc PAOP and PADP 2/2 ischemia induced inc in LVEDP
30
Q

Induction for thoracic aneurysm repair?

A
  • all of the normal stuff, place invasive monitoring preinduction
  • ensure adequate BBlockade to dec risk of MI/aortic rupture/propagation
  • obtain baseline set of vitals, PAC data, evoked potential signals
  • apply cricoid pressure
  • carefully titrated, high narcotic IV induction w/goals of avoiding HD instability, tachy, brady (this pt also had AR)
31
Q

Things to think about re: maintenance of anesthesia for thoracic aneurysm repair?

A
  • TIVA (or limit gas d/t MEP/SSEP, keep steady throughout
  • HR between 60-80 (this pt also had AR)
  • CI 2-2.5
  • SBP 100-115, MAP 100 above Xclamp, 50 distal to Xclamp
  • various short acting vasoactives ready (NTG, nicardipine, esmolol, nitroprusside)
32
Q

Some interventions you could do if SSEP signals dec amp and inc latency ater surgeon applies X clamp for thoracic aneurysm repair?

A
  • optimize HD: MAP, normocapnia, acidosis, check ABG
  • ask perfusioninst to inc flows
  • reposition X clamp
  • ensure mild hypothermia at 30-34C (aortic arch/asc aortic sx requires deep hypothermic cardiac arrest 15C)
  • w/d 10-20cc of CSF from lumbar drain
  • consider steroids, naloxone, Mg, CCBs (potentially dec incidence of spinal cord ischemia)
33
Q

Some complications of CSF drainage from lumbar drain?

A
  • H/A, meningitis
  • spinal/epidural hematoma
  • intracranial bleeding 2/2 tearing of cerebral bridging vessels
  • persistent CSF leak
34
Q

Xclamp release during thoracic aneurysm repair causes hypoTN. Why? Two reasons

A
  • central hypovolemia –> dec in cardiac preload
  • distal tissue ischemia –> vasoactive mediator release –> dec in SVR and inc in capillary permeability and loss of intravascular fluid + inc in PVR
35
Q

What medications can help you “volume load”? Give an example of when you’d want to do this

A
  • vasodilators like nitroprusside or NTG
  • could admin these when patient has X clamp on aorta (like for thoracic aneurysm repair) to facilitate pumping pt full of fluid), but need to dc them before release of clamp obviously (since they’ll have “central hypovolemia” + vasoactive mediators released after clamp comes off –> hypoTN)
36
Q

Preop eval of patient with previous heart transplant?

A
  • discuss w/transplant team re: cardiac status, immunosuppression, abx ppx need?
  • review recent echo, angio results
  • assess for rejection signs: arrhythmias, fever, malaise, SOB
  • ID and eval PM (usually require for bradydysrhythmias)
  • ECG
  • ID complications from immunosuppressive tx: BM suppression, osteoporosis, hepatotoxicity, opportunistic infx
  • admin stress dose steroid
37
Q

What’s the deal with heart transplant patients and their denervation?

A
  • lack of autonomic innervation –> can’t respond to acute hypoTN by inc HR, so instead relies on adequate preload to maintain CO
  • response to circulating cats is normal though
  • HR response to normal resp variations, carotid sinus massage, valsalva, oculocardiac reflex ==> all absent
  • absent vagal influences cause relatively high resting HR (90-120)
38
Q

Who do you admin ppx abx to dec bacterial endocarditis?

A
  • MVP alone is NOT an indication
  • prosthetic valve
  • previous IE
  • unrepaired cyanotic CHD or 6 mo after repiared
  • cardiac tx pts who develop valvulopathy
39
Q

Differences in anesthetic goals for patients with MR vs MR 2/2 MVP?

A

In essence, you want to avoid everything that can cause more ventricular emptying –> worsens MVP –> inc MR

40
Q

Complications a/w/ expanding aneurysm?

A
  • rupture and exsanguination
  • dilation of aortic root –> AR, cardiac tamponade, hemothorax, occlusion of arteries arising from aorta
  • compression of proximal structures –> diff intubation (tracheal/bronchial compression), SVC syndrome, hoarseness (L RLN)
41
Q

Brief summary of Crawford classifications for thoracoabd aneurysms?

A
42
Q

What is an endoleak?

A
  • failure to completely isolate aneurysmal sac from arterial blood flow
  • particularly bad bc potential for pressurization of sac (endotension) –> aneurysmal enlargement –> rupture
  • five types described (see pic)
43
Q

What do Q waves signify?

A
  • often in normal EKGs
  • pathological if bigger, wider, and found in leads where they aren’t supposed to be
  • I think that they usually signify past MI. Axis deviation can also hint at this
44
Q

Who might it be reasonable to start periop BB tx on?

A
  • 2-7d preop in pts w/:
    1) 3 or more RCRI risk factors (DM, HF, CAD, renal insuff, CVA), or
    2) int or high risk MI IDed by preop risk stratification tests
45
Q

What are the ACC/AHA guidelines for getting preop TTE?

A
46
Q

Pros/cons of labor vs C/S for patient with cardiac issues?

A

Labor:
- physical stress throughout
- hyperdynamic circ changes that occur at delivery

CS:
- significant cardiac stress (CO inc up to 50% during CS)
- inc blood loss
- higher risk of infx
- delayed ambulation
- inc postop pain

…If develops preE w/severe features or eclampsia, proceed to CS

47
Q

Cardiac effects of Mg administration (for preE, etc in OB)?

A
  • hypoTN, brady, heart block, cardiac arrest
  • discuss pros/cons w/OB if have pt w/cardiac issues + eclamptic stuff
  • monitor closely for s/s of toxicity (reflex loss, hypoTN, CNS change, resp depression, EKG changes)
  • if any of these, d/c immediately, check Mg level, give diuretic to inc excretion, give CaGlu to antagonize effects
48
Q

What is a pt at inc risk for if hypertensive preop? What to do?

A
  • HD instability
  • intra-op end organ ischemia (MI and stroke)
  • arrhythmias
  • CHF

Should:
- do H&P to ID cause of HTN, other CV risk, e/o end organ damage or current sxs
- review current therapy
- get EKG, lytes, BUN/Cr to eval for EOD
- r/o causes of HTN in young adult: illicit drugs, hyperthyroid, pheo, coarctation

Reasonable to delay elective case by 6-8 weeks to optimize BP if > 180/110, e/o EOD, or undergoing cardiac/carotid/pheo surgery

EOD examples: LVH, angina, MI, CHF, CAD, stroke, TIA, CKD, retinopathy, PAD

49
Q

Factors that lead to/exacerbate LV outflow tract obstruction (HOCM)?

A

Anything that decreases LVEDV!

  • Hypovol (dec preload)
  • Sympathectomy/vasodilation (dec SVR/afterload)
  • Inc myocardial contractility (inc LV emptying)
  • Tachycardia (dec diastolic filling time), dysrhythmia
  • Excessive PPV/PEEP (dec preload)
  • Inadequate LUD (dec preload, for preggo)
50
Q

Two examples of things that could under or over-estimate severity of AS?

A
  • under: dysfxnl LV can lead to dec aortic transvalvular gradient as compared to normally fxning LV
  • over: hyperdynamic circulation
51
Q

Why is a dec in SVR for someone w/AS poorly tolerated?

A
  • usually dec in afterload promotes inc CO, but here the stenotic valve (instead of the SVR) creates most of the afterload on the ventricle
  • so, significant drop in SVR is bad here bc they have a relatively fixed SV and can’t inc their CO
  • leads to subsequent diastolic hypoTN and compensatory tachy in a pt w/hypertrophied myocardium –> at risk for subendocardial ischemia
52
Q

Can you give protamine to reverse effects of LMWH?

A
  • not recommended bc doesn’t reliably reverse
53
Q

ACC/AHA guidelines on starting BB periop?

A
  • Harmful to start BB on day of surgery (inc risk of brady, hypoTN, stroke, overall mortality)
  • MIGHT be ok to start 2-7d prior in high RCRI risk (3) pts
54
Q

Physiologic effects of beach chair position on anesthetized pt?

A
  • an awake pt, will dec CPP (15%), SV, CO. But partially compensated for by inc in SVR
  • under GA, this is inhibited –> at risk for cerebral ischemia
  • if DMT2 and s/s of AN –> even worse!
55
Q

What’s the significance of LBBB?

A
  • more significant a/w/ ischemic heart dz, aortic valve dz, LVH , CHF, HTN than does RBBB
  • dx of MI difficult bc BBB pattern hides ST and T wave findings
  • widened QRS makes mistaking SVT for VT more likely
  • PAC placement can –> 3* block (d/t transient RBBB)
56
Q

A couple of considerations re: type of stress tests indicated for particular pts?

A
  • dobutamine should be avoided in pts w/severe HTN, serious arrhythmias, or hypoTN
  • shouldn’t suggest exercise if pt unable to cooperate for variety of reasons
  • exercise unacceptable in pts w/LBBB bc very unspecific (HR elevation –> septal motion abnl in LBBB –> dec coronary perfusion, but this induced perfusion defect not actually r/t/ ant desc artery disease)
  • adenosine or dipyridamole w/nuclear imaging should be avoided in pts w/critical carotid dz, risk for bronchospasm
  • exercise EKG utilized for most ambulatory pts
57
Q

Potential causes of PM loss of capture? What to do?

A
  • MI (lengthens refractory period + inc energy requirement to depol)
  • lyte abnlties (raises depol threshold)
  • lead failure
  • acid/base disturbance
  • attempt to fix any of the above, consult cardiologist, and transcutaneously/transvenously pace
58
Q

Steps to take if patient develops VT?

A
  • assess unstable vs stable
  • if unstable, assess if wide complex, irregular (unsync) cardioversion vs any other (sync)
  • if stable, adenosine to tx or at least slow down. Then procainamide vs amiodarone
  • ID and correct any: hypoxemia, hypovol, hypercapnia, hypo/hyperK/Mg/thermia/glycemia, PE, acid/base
59
Q

When would you admin bicarb during code?

A
  • may actually worsen acidosis (usually resp acidosis during initial stages of code) since bicarb + H –> CO2
  • but, significant acidosis –> CV dep (dec contractility, vasodil –> hypoTN), inc risk of arrhythmias, resistance to inotropic + vasoconstrictive effects of pressors
  • therefore, would give if 1) preexisting met acidosis, 2) hyperK, or 3) if pH remained <7.2 despite 5-10 mins of resuscitation
60
Q

Roller pump vs centrifugal pump for CPB?

A

Roller:
- nonsensitive to preload/afterload
- delivers pulsatile flow
- delivers certain amount of flow based on pump speed
- inc damage to RBCs
- potential large air embolus delivery
- risk of over-pressurization (d/t lack of sensitivity to change in afterload)

Centrifugal:
- rotation force –> forward flow
- sensitive to changes in pre/after load
- doesn’t deliver pulsatile flow
- less damage to RBCs
- cease to fxn if air entrained

61
Q

alpha vs pH stat?

A
  • alpha stat shown to have improved neuro outcomes in adults undergoing mod hypothermic CPB. For deep, unknown. For kids, better w/pH stat (brain injury thought r/t ischemia so more blood flow = good bc this facilitates cerebral cooling before CV arrest –> brain protection)

alpha: CO2 NOT added, despite dec in PP of CO2 that occurs w/hypothermia (inc solubility of CO2). Likely better bc neuro events usually 2/2 embolic events vs ischemia, so the added CO2 leading to more cerebral blood flow can cause more harm than good

  • pH stat: add CO2 PRN to maintain pH of 7.4 and PaCO2 of 40
62
Q

What to do if pt goes into afib intraop?

A
  • if stable and not super reliant on NSR (atrial kick), can just rate control (BB, CCB) and monitor BP closely
  • if signs of ischemia, persistent hypoTN, etc would consider pharmacologic (amio) or DC cardioversion
  • if all fails, CPB (if in a cardiac case)
63
Q

What’s the point of vigorous inflation of lungs s/p CPB?

A

1) recruits collapsed alveoli
2) PPV –> inc blood flow through pulm vasc (I think 2/2 inc preload 2/2 inc intrathoracic pressure) –> displaces air into L heart where can be more easily removed w/a vent

64
Q

Name a few reasons for LV failure s/p CABG and MVR (for MR)?

A
  • inc afterload 2/2 MVR (LV having to work a lot harder now that the low resistance flow backward into atrium no longer present)
  • graft failure (kinking, air, clot) of CABG
  • inadequate myocardial preservation during CPB
  • inadequate coronary blood flow (hypoTN, coronary emboli, spasm, tachycardia)
  • MI, valve failure, hypoxemia, inadequate preload, reperfusion injury, acidemia, lyte abnlties
65
Q

Difference between radial and central pressures immediately s/p CPB?

A
  • peripheral vasodilation 2/2 rewarming –> radial can be 30mmHg lower than central!
  • usually resolves w/in 45 mins
  • surgeon can directly palpate aorta or connect transducer to aortic vent or needle inserted into aorta
66
Q

What is pulsus paradoxus?

A
  • exaggeration of nl variation in systolic P and pulse that occurs during inspiration
  • nlly, inspiration –> more negative intrathoracic P –> inc venous return to the heart –> inc RV volume –> bulging of IV septum toward LV –> dec capacity –> dec SV and SBP –> inc in HR 2/2 baroR reflex
  • this nl variation of BP can be exaggerated in tamponade, airway obstruction, COPD, PE
67
Q

Mech of diltiazem?

A
  • dec rate of SA node and slows conduction through AV node
  • also has some negative inotropic effects, but less so than verapamil
  • preferred drug in pts w/systolic HF
68
Q

Indications for catheter ablation?

A
  • SVT d/t AVNRT
  • WPW, unifocal a tach, a flutter
  • a fib w/lifestlye impaired sxs and inefficacy/intolerance of antiarrhythmic agents
  • symptomatic VT
  • patient preference/noncompliance
69
Q

Common causes of TR?

A
  • Pulm HTN (e.g. from MS) –> RV overload –> RVH –> eventually, RV dilation –> TR
  • Ebstein’s anomaly
  • infective endocarditis
  • carcinoid syndrome
  • tricuspid valve prolapse
70
Q

A few reasons why PM might not be capturing?

A
  • MI (inc energy requirement for depol)
  • lead dislodgement
    delivery of insufficient energy
  • PM malfxn
  • acid/base disturb
  • lyte abnlties