Case 10 - non cardiac surgery after heart transplantation Flashcards
explain the physiology of transplanted heart? is the heart denervated? what remains in tact?
Transplanted Heart
-
Denervated -> does not respond to autonomic nervous system
- (no response to symp or parasymp stim)
-
intrinsic myocardial mechanisms and reflexes remain in tact
- able to respond catecholamines (directly) through myocardial receptors
what are the results of cardiac denervation - Does the heart respond to valsalva, change in BP, ephedrine, intubation? What is the normal heart rate?
Results of cardiac denervation:
1) lack of vagal tone -> HR 90 - 100 bpm
2) no response to autonomic reflexes
- no change in HR with hypotension, HTN, valsalva, carotid massage.
- no efferent baroreceptor response
3) no response to drugs that work indirectly on autonomic nervous system
-
no HR response to vaglytics
- atropine, panc, meperidine
- no HR response to vagotonic
- acetylcholinesterase inhibitor, opiods)
4) HR responds only to drugs that have direct effect
- digoxin has both indirect and direct. no response to indirect, but good response to direct.
- dig maintains positive inotropic effects, but does not slow HR rate via parasymp mediated effects on AV node
5) decrease symp response to laryngoscopy, intubation, light anesthesia, painful stimuli
* prolong exposure however leads to inc circulating catecholamines - > tachycardia
what intrinsic myocardial mechanisms remain intact - response to catecholamines, response to inc preload, coronary blood flow in response to pH?
Intrinisic myocardial mechanisms
REMAIN INTACT
1) b1 and b2 receptors of graft myocardium are functional
- respond to catecholamines, and direct acting sympathomimetic agents
- epi, norepi, isoproternol, dobuatmine
2) frank-starling mechanism is functional
- inc preload leads to inc SV
- this is the primary mechanism of increasing CO in response to stress or exercise.
-
**only way patients can inc CO in the face of a fixed HR is to inc SV via inc preload**
- eventually, prolong stress leads to inc catecholamines, which inc HR - > inc CO
3) metabolic regulation of coronary blood flow in response to pH and CO2 = intact
*
can reinnervation of transplanted heart occur?
not enough literature
at this moment, reinnervation of transplanted heart does not occur in the first few years after transplant
what are your anesthestic concerns for patietns taking immunosuppresive therapy?
- immunosuppresive agents have many side effects
Cyclosporine
- nephrotoxicty, hepatoxicity
Azathioprine
- thrombocytopenia
- anemia
- leukpenia
corticosteroids
- HTN
- DM
- adrenal insufficency
- psych disturbances
Anesthseia
- **need to look at every system to see their functin: lung, kidney, CNS, liver. **
- BUN/Cr, CBC, PLT, Coags, LFTs, electrolyte
what are your preanesthetic concerns for a heart tx patient? (rejection, immunosuppresant SE, CAD, arrythmias, angina and MI, dec CO and preload)
1) patient in rejection or no rejection
- rejection -> deteriorating ventricle function, may need to consider ECHO
2) accelerated CAD
- possibly due to vasculitis form subclinical rejection
- patients do not experience angina during MI (denervation of autonomic nervous syst)
3) arrythmias
- common in tx heart: 1 AVB, RBBB, PAC
- significant arrythmias = sign of acute rejection
4) immunosuppresant SE
- liver and kidney dysfunction, thrombocytopenia, pancytopenia, electrolyte derangements
5) steroid therapy - may require stress dose
6) frank starling mechanism
* CO is dependent on preload since HR is initially fixed (delayed increase of HR 2/2 inc of circulating catecholamines)
what anesthetic techniques are applicable to patients with heart transplant? (different modes of anesthesia, meds to give at induction, neuromuscular blockade, volume depletion management)
if no rejection and graft function is good, treat heart tx as normal patients
- general, spinal, epidural, regional, and local are all acceptable
considerations in heart tx pts
1) normal induction meds is well tolerated during general
2) neuromuscular blockade can be augmented by cyclosporine and antagonized by anticonvulsants
-
okay to use, close monitor via nerve stim
3) Hypotension management - volume depeltion and acute vasodilation (ex spinal) poorly tolerated b/c NO REFLEX TACHY
-
frank-starling mech intact –> give Fluids to maintain SV -> inc CO
- eventually inc catecholamines in blood results in tachycardia (delayed response due to no initial sympathetic reflex)
what intraop monitors do you use for heart tx patients?
if no rejection and graft function is good, treat heart tx as normal patients
standard ASA
consider invasive monitoring only if indicated 2/2 surgical factors (HD instability bound to happen during surgery, fluid loss, blood loss)
What emergency meds would you give for, **dec HR, dec contractility, dec SVR? **
recall - denervated heart
- no response to autonomic nervous system
- intact B adrenergic receptors
1) Decrease HR (chronotropy)
- Direct acting chronotropic agents - epi, isoproternol, dobutamine
- transcutaneous or transvenous pacing
- **ATROPINE WILL NOT WORK** (anticholinergic response)
2) dec contractility (inotropy)
* Epi - direct acting inotropic agent of choice
3) dec SVR
- has nothing to do with denervated heart
- phenyl, norepi, vaso = all work on vasculature directly and have nothing to do with heart
Would you consider using dopamine or ephedrine in emergency situations?
NO
Ephedrine
- indirect and direct actions on alpha and beta adrengeric receptors
- indirect effects 2/2 enhanced release of Norepi
- release of Norepi takes time thus not first-line emergent drug
dopamine
- direct and indirect effects
- immediate precursor of and causes release of norepinephrine
- works on dopamine, alpha, and beta adrenegic receptors
- vasoconstrictive (alpha), and inc contractility and HR (beta) is dose dependent
- alpha and beta adrenergic effects only come from released norepinephrine = takes time for release -> not first choice
you are done with the case, and now you want to antagnoize your neuromusuclar blockade. Do you need to give an anticholinergic (glyco) along with neostigmine
Yes
- although you will not get bradycardia with neostigmine, you still want to give glyco to avoid noncardiac cholinergic side effects (like bronchospasm)
