Cardiovascular Flashcards

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1
Q

Heart Transplant Recipient:

Considerations:

A
  1. Denervated heart (no sympathetic or parasympathetic innervation):​​​
    • Delayed response to circulating endogenous catecholamines (decreased or no sympathetic response to laryngoscopy, pain)
    • Preload-dependent
    • No vagal influence, resting HR 90 to 100 (carotid massage has no effect on HR)
    • Prone to dysrhythmias (PPM in 20%)
  2. Pharmacology Considerations:
    • Poor response to indirect sympathomimmetics (eg. ephedrine)
    • Intact response to direct-acting sympathommimetics
  3. The Allograft:
    • Can undergo rejection - decreased EF
    • Accelerated CAD
    • Silent ischemia 2o to denervation
    • Endocarditis prophylaxis IF there’s a valvulopathy
  4. Immunosuppressive Therapy:
    • Increased risk of infections (eg. cholecystitis)
    • Strict aseptic technique
    • Stress dose corticosteroids if chronic use
    • Potential SEs: HTN, renal impairment, malignancy
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2
Q

Heart Transplant Recipient:

Pre-op visit:

A
  1. Thorough review of functional capacity:
    • How are the other organs functioning?
  2. Sides effects of immunosuppresant medications?
    • Renal failure (Tac, cyclosporin A)? - Crt
    • HTN (steroids, tac, cyclosporin A)?
    • DM (steroids, tac, cyclosporin A)? - Glucose
    • Anemia or thrombocytopenia (MMF, azathioprine)? - CBCd
    • Liver dysfunction? - transaminases, INR/PTT
  3. Graft function? :
    • If elective surgery, must rule graft dysfunction out to reduce morbidity
      • Hx, P/E: CHF? Dysrhythmias? (late signs)
      • Investigations: Biopsy results (early sign), echo, dobutamine stress echo. Cannot do excercise stress test as limited by HR response.
    • Dysrythmias?
      • ECG, holter
      • Lytes: K, Mg
      • PPM/ICD? Function?
  4. Accelerated CAD?
    • Most common symptom = dyspnea
    • ECG : may show both donor and recipient P waves (SA node x 2). Look for signs of ischemia.
  5. Infection?:
    • Any signs ANYWHERE?
    • Do not present with typical signs
  6. Consider consultation with transplant clinic & cardiology pre-operatively
  7. If valvulopathy: Infective endocarditis prophylaxis
  8. Measure blood levels of immunosuppressives periop
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3
Q

Heart Transplant Recipient:

How would you do the anesthetic?

A
  1. Choice of anesthetic: both GA or neuraxial okay, BUT if neuraxial, must check plts, INR/PTT
  2. Equipment: 5-lead ECG, consider art line based on surgery, glucometer
  3. Maintain these hemodynamic goals:

Preload: maintain normal or high (CO increases by increasing stroke volume)

Rhythm: avoid pro-arrhythmic states

Afterload: maintain, to ensure perfusion to potentially ischemic myocardium (accelerated CAD common) Contractility: Maintain. Avoid myocardial depression.

  1. Depth of anesthetic: Assess with BP, not HR
  2. Have direct-acting sympathomimetics present (epinephrine). Do not use indirect-acting agents.
    • Atropine and panuronium: no effect
    • Neostigmine: May cause bradycardia (direct and indirect), may not. Still need to reverse with neo/glyco to counteract peripheral muscarinic effects
    • Adenosine: Increased effect
  3. Avoid infection:
    * Strict sterile technique & minimize catheters/invasive devices
    * Oral over nasal ETT if choice
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4
Q

Heart Transplant Recipient:

How would you do the anesthetic in a pregnant patient?

A
  • Same goals as non-pregnant state apply
  • Epidural is very good technique, but:
    • Look at coags first
    • Slow titrated epidural helps to prevent hypotension
    • Fluid bolus first
    • Treat hypotension with small Phenyl boluses
  • GA also acceptable
  • Ensure adequate intravascular volume
  • Extra attention to aseptic techniques
  • Anti-rejection drugs have no adverse effects on fetal or neonatal outcomes
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5
Q

HOCM:

Considerations?

A

HOCM:

Considerations:

  1. Dynamic LVOT obstruction (25% at rest, most only during exertion, others have no obstruction at all)
  2. Mitral Regurgitation
  3. Hypertrophy : Diastolic dysfunction & Ischemia
  4. High risk of arrythmias, risk of sudden death
  5. CPR minimally effective
  6. Medications:
    • Beta-blockers or CCBs
    • Anti-arrythmics (amiodarone, disopyramide)
    • Anticoagulants (warfarin)
  7. PPMs or AICDs - primary if high risk or secondary
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6
Q

HOCM:

Pre-Op Assessment?

A

History:

  • Screen for LVOT obstruction (mostly on exertion):
    • Dyspnea on exertion? (very common)
    • Pre-syncope or syncope, esp when standing up?
  • Screen for hypertrophy:
    • Chest pain (1/4 of pts)? Esp. w/ heavy meals.
  • Screen for arrhythmias:
    • Heart palpitations?
  • Family history of Sudden Cardiac Death?

P/E:

  • CVS and Pulm only.
  • CVS:
    • Harsh crescendo-decrescendo systolic murmur
      • From LVOT obstruction or MR
      • Is it accentuated with the Valsalva maneuver? Going from squatting to standing? (decreasing SVR and preload)
      • Does it become less intense with handgrips or leg raising? (increasing SVR, then preload)
    • S4 (stiff ventricle)
  • Pulm:
    • Crackles, rales due to pulmonary congestion

Labs: None.

Imaging:

  • EKG:
    • LVH
    • Prominent Q-waves in inferior and lateral leads common (accentuation of normal septal depolarization)
    • LAD
  • Echo:
    • Hypertrophy: Variable patterns. Septal, apical, LV free wall, RV.
    • Resting LVOT obstruction present in only 25% of pts
    • MR - secondary to SAM
    • Diastolic dysfunction
  • If Echo suboptimal, MIBI or Cardiac MRI
  • Also, consider cardiac catheterization if you want to assess the severity of LV obstruction.
    • 3 factors to measure: CO, LVOT pressure gradient and LAP (LV filling pressure)
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7
Q

HOCM:

Pre-Op Optimization?

A
  • LVOT obstruction:
    • Very severe? Is the OR elective? Consider surgical procedure:
      • LV myectomy (if NYHA III or IV or recurrent syncope, gradient >50mmHg at rest)
      • Alcohol ablation of septal perforators (non-surgical)
      • MV replacement, plication
    • Ensure adequately beta-blocked or calcium-channel blocked long-term.
    • Is there a fluid deficit? Pre-induction bolus
    • Give benzo. Prevent anxiety-induced sympathetic stimulation.
  • If significant SOBOE or clinical CHF, consider judicious diuretics - be very careful to maintain preload though
  • Arrythmias:
    • Pacemaker ONLY if SA node dysfunction or AV block
    • Does pt require medical control of arrythmias - amiodarone
    • Or AICD prior to OR?
    • Have transcutaneous / transvenous pacing immediately available
  • Anticoagulation:
    • If paroxysmal or chronic A. Fib
    • If on coumadin: reverse, hold or convert to heparin
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8
Q

HOCM:

How would you do the anesthetic?

A

Goals:

  • Preload: HIGH
  • Afterload: increased
  • Contractility: depressed
  • Rhythm: STRICT sinus rhythm
  • Avoid: tachycardia, inotropes, vasodilators

First Rx for hypotension = fluid/fluid/fluid!

Second Rx = vasoconstriction with pure alpha-agonist: phenylephrine

Third Rx = Decrease contractility : increase volatile

Options:

Either GA or neuraxial but be very careful with neuraxial. Need to make sure that hemodynamic goals met. Spinal may be dangerous, as with in AS, so consider titrated epidural instead. Keep preload high with fluid boluses, afterload high with phenyl infusion, and make sure BP doesn’t drop to prevent reflex tachycardia.

Meds:

  • Alpha agonists (phenylephrine) to maintain SVR
  • Beta-blockers or CCB for negative ionotropy
  • Anti-arrythmics (amiodarone)

Monitoring:

  • Full hemodynamic monitoring to ensure hemodynamic goals are met:
    • 5-lead EKG
    • Art line
    • IJ central line for CVP monitoring
  • Immediate availability of pacing and cardioversion pads

GA:

Induction: Anxiolytic, deep plane of anesthesia prior to airway manipulation.

Maintenance: Volatiles great as they have myocardial depressant properties. But, be wary of arrhythmogenic potential

Emergence: Similar to Induction, avoid sympathetic activation.

Disposition:

  • Pain control: Must be good. Either PCA or titrated epidural with good monitoring (avoid hypotension) to avoid SNS activation.
  • If major surgery, large potential for pain or fluid shifts, admit to a High Dependency Unit.

Kaplan:

PA Catheter: As in valvular AS, the information provided by insertion of a PAC is worth the small arrhythmogenic risk. The potential for hypovolemia-induced exacerbation of outflow tract obstruction makes it crucial that the clinician have an accurate gauge of intravascular filling. The reduced diastolic compliance means that the PCWP will overestimate the patient’s true volume status, and a reasonable clinical objective is to maintain the PCWP in the high-normal to elevated range.

Have phenylephrine ready: “it’s almost always a low-risk, high-yield choice for the hypotensive patient with HCM. It augments perfusion, may ameliorate the pressure gradient, and often elicits a potentially beneficial vagal reflex when used to treat tachyarrhythmia-induced hypotension.”

Hypotension is almost always the result of underlying hypovolemia. In most cases, a beneficial response can be obtained with aggressive replenishment of intravascular volume and concurrent infusion of phenylephrine.

**Inotropes, β-agonists, and calcium are all contraindicated because they worsen the systolic obstruction and perpetuate the hypotension. Get paradoxic responses.

The inhalation anesthetics commonly are used for patients with HCM. Their dose-dependent myocardial depression is ideal because negative inotropy reduces the degree of SAM-septal contact.

Several investigators have suggested that regional anesthesia, with its potential for accentuating peripheral vasodilation, may be relatively contraindicated in the management of patients with HCM. The theoretic constraints are similar to those for patients with valvular AS, and the same clinical caveats apply. If the vascular system is kept appropriately full and “tight” with vasopressors, it is reasonable to consider these techniques in the light of other clinical advantages they might offer the patient. Catheter techniques (e.g., continuous spinals, epidurals) may be preferable to the bolus administration of local anesthetics to achieve a finer degree of control of the anesthetic level. There unquestionably is the potential for a cascade of iatrogenic complications if sympatholytic hypotension is treated in a knee-jerk fashion with ephedrine, epinephrine, or a variety of other equally contraindicated β-adrenergic agonists.

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9
Q

HOCM

How well do these patients tolerate pregnancy?

How would you optimize the patient’s status if seeing in PAC?

How would you do the anesthetic in a pregnant patient?

A

Preamble (Chestnut): Most women with HOCM tolerate pregnancy well, but there is a close correlation with preconception functional status. If asymptomatic pre-conception, there is a low risk of worsening their clinical condition. If they were symptomatic, there is a much higher chance of deterioration.

How pregnancy affects hemodynamic goals of HOCM:

  • The greater blood volume of pregnancy helps maintain preload, which reduces LVOT obstruction. :) But aorto-caval compression can reduce preload. :(
  • However, pregnancy increases HR, contractility and decreases SVR, which worsen LVOT obstruction. :(

Optimization:

  • Ensure Beta-blockade is continued throughout pregnancy
  • Consider implantation of a PPM or AICD if women of childbearing age are a) symptomatic, or b) have a history of syncope or presyncope

Tolerance of Labour:

  • C-section reserved for obstetrical indications
  • Typically tolerate the second stage of labour well, as SVR increases

Specifics of Anesthetic Management:

  • Maintain Beta Blockade during labour and delivery, man!
  • Epidurals and Combined Spinal-Epidurals are acceptable, however vasodilation must be prevented with phenylephrine (the preferred vasopressor in HOCM)
  • Single-shot spinal is a relative contraindication, because of the rapid onset of sympathectomy
  • Oxytocin: Decreases SVR, so important to give SLOWLY
  • Methylergonovine may be a good alternative
  • Anesthetic hemodynamic goals remain the same as in a non-pregnant patient. However, to maintain preload, must also make sure to prevent aorto-caval compression!
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