Heart transplant including blue book article Flashcards
What happens to the nerve supply of the transplanted heart?
Absence of sensory, PSNS (from vagus) or SNS (stellate ganglion) innervation- surgically dissected.
Direct-acting vasoactive meds therefore useful but not indirect-acting (responds to circulating catecholamines in an attenuated manner so have blunted responses to exercise, pain & hypovolaemia)
Maximal HR, HR variability & contractility are reduced but coronary autoregulation remains intact
What happens to the nerve supply of the transplanted heart? consequences?
Absence of sensory, PSNS or SNS innervation.
Can’t respond to indirect-acting agents (ephedrine) or peripheral stimuli to induce haemodynamic changes (eg. carotid massage, laryngoscopy, valsalva)
Direct-acting vasoactive meds therefore useful but not indirect-acting.
However, B effects of epinephrine & norepinephrine are exaggerated; reserve for refractory cardiogenic shock
What’s the resting HR for the transplanted heart? why?
Generally higher- 90-100bpm than native heart due to loss of predominant vagal tone in normal hearts; goes to “default rate”, HR may vary depending on age of graft
do atropine & glycol work on transplanted heart?
No- ineffective in treating bradycardia as heart has lost PSNS innervation.
atropine & glycol still retain effects on non cardiac tissues
What may the ecg show in the transplanted heart?
- 2 p waves; one from residual native atrial cuff tissue & one from implanted atrium
- atrial arrhythmias- eg. 25% develop atrial flutter or fibrillation- lack of vagal tone & increased endogenous catecholamines (conduction delays are the most common arrhythmias in transplanted heart. suture lines predispose to heart blood, ventricular arrhythmias are rare- may be a marker of acute rejection or CAV)
- R) BBB due to frequent endomyocardial biopsies (5-10% have R) BBB)
- bradyarrhythmias common (10% require PPM)
What are the haemodynamic considerations for the transplanted heart?
resting HR 90-100
HR response to exercise is blunted, slower to respond
CO drops during exercise
no diurnal variation in BP is seen
no effect with carotid sinus massage & valsalva
in response to drop in preload, no tachycardia response- relies on preload & slow riske in circulating catecholamines to incr HR in response to hypotension
Atrial contraction is asynchronous & atrial filling is impaired, esp LA
Transplanted heart is preload-dependent & relies on adequate intravascular volume; starling response is retained & this becomes important for increasing SV.
Avoid hypoT, VD & acute preload decreases (slow induction, generally avoid neuraxial as denervated heart doesn’t reflexively compensate for haemodynamic changes- any neuraxial pretreated with IVT, very slowly titrated with direct-acting vasopressor running).
No HR response (eg. the Anrep effect of normal heart) to incr afterload
Cognisant that vasodilator drugs (eg. GTN, hydralazine) may have profound effect as no reflex compensatory SNS response- so very carefully titrate propofol with direct-acting vasopressor (metaraminol, phenylephrine) running
Which vasoactive medications are useful for the transplanted heart?
what need to be careful of though?
direct-acting as intrinsic alpha & B receptors in the grafted heart are intact, eg. Adrenaline
The effects of NAdr, Adr & dobutamine may be exaggerated due to increased adrenoceptor density
What are some side-effects of long-term immunosuppression?
renal dysfunction
What should the preop evaluation focus on for heart transplant?
- cardiac functional status
- S&S of heart failure
- signs organ rejection (highest frequency in the first 3/12- SOB, fever, anuria/oliguria, fatigue, fluid retention & weight gain, cardiac allograft vasculopathy)
- medications: if on long-term corticosteroids (equivalent 5mg PO pred/day) consider 100mg IV hydrocortisone preop
How treat bradyarrhythmias in the transplanted heart?
direct-acting chronotropic agents (isoprenaline, adrenaline) or electrical pacing
while neostigmine won’t cause bradycardia, what’s a rare complication of it’s administration in heart transplant?
may cause advanced bradycardia, HB & asystole especially if >6/12 post-transplant (reinnervation can occur slowly- SNS innervation at 6-8/12 & PSNS innervation at 1-3yrs post-transplant- variable, unpredictable, LV first & RV later if at all)
what effect does digoxin have on the transplanted heart?
no rate-controlling effect but retains inotropic effect
can adenosine be given to a heart transplant pt?
no; profound & prolonged bradycardia effect on a denervated heart
Is the starling effect retained in the denervated heart?
Yes; it responds to increases in preload with increased SV & CO
Monitoring for heart transplant pt?
5-lead ecg
art line
consider more monitoring (CVC, TOE, rarely PAC) if significant blood loss or large IV volume shifts anticipated, particularly if pt has evidence of cardiac dysfunction- R) IJ may have significant scarring
Do pts with heart transplant have the classic presentation during episodes of myocardial ischaemia?
No- as no visceral innervation
High index of suspicion for MINS postop
do pancuronium & sux impact the HR of a pt with heart transplant?
No, but retain extracardiac effects
Principles of analgesia in heart transplant patients?
important to attenuate any SNS surges perioperatively (high risk perioperative myocardial ischemia, particularly if allograft vasculopathy)
use multi-modal analgesia incl regional
Likely to avoid NSAIDs as high risk renal impairment &HTN
Use BIS with GA to titrate depth
Principles of analgesia in heart transplant patients?
important to attenuate any SNS surges perioperatively (high risk perioperative myocardial ischemia, particularly if allograft vasculopathy)
use multi-modal analgesia incl regional
Likely to avoid NSAIDs as high risk renal impairment &HTN
Use BIS with GA to titrate depth
After what time has the risk of acute rejection diminished post-transplant?
12/12, the pt usually stabilised on an immunosuppressive regimen
What are the considerations wrt immunosuppression in the heart transplant pt?
- Early post-transplant (within the first 3-6/12), risk of immunosuppression-related complications is higher given that high therapeutic levels are targeted, early complications incl: renal dysfunction from calcineurin inhibitors (cyclosporine, tacrolimus), steroid-induced diabetes, steroid-induced myopathy, leukopenia, gingival hyperplasia with cyclosporine, lowering of seizure threshold with calcineurin inhibitors.
- liaise with pts heart transplant team (multi-D), esp within the first 6-12/12 post-transplant- consider periop immunosuppression regimen & adrenal suppression prophylaxis
- Ideally, pt should be on a stable immunosuppressive regimen prior to elective surgery
- risk of acute rejection has diminished after 12/12; primary concerns from this time include allograft vasculopathy (fibrous intimal hyperplasia, the predominant risk for graft dysfunction & chronic rejection in the late post-transplant period), may cause ventricular dysfunction & such pts are @ higher risk for myocardial ischaemia, volume overload or arrhythmias.
- later, there’s risk of malignancy with chronic immunosuppression incl post-transplant lymphoproliferative disease (may involve airway)- lymphoma more common with a prognosis of under 30% survival @ 5yrs.
- more than 10% of heart transplant recipients develop de novo malignancy in the first 1-5yrs after transplant (3-4x > background risk), with skin cancers 100-fold incr incidence cf controls. Need rigorous screening for SCC.
- increased risk infection- ABx prophylaxis, meticulous aseptic technique
- adrenal suppression prophylaxis: hydrocortisone 100mg at start of surgery followed by infusion 200mg/24hrs, hydrocortisone 100mg/24hrs IVI while NBM, restart usual glucorticoid once eating & drinking if recovery uncomplicated, otherwise double dose for up to 1/52
What are some common medical comorbidities in heart transplant pts & how this impacts periop Mx?
they may be on anticoagulants, may have an ICD that needs interrogation/reprogramming
renal: eg. nephrotoxic immunosuppression (calcineurin inhibitors), repeat exposure to contrast0 Ax baseline Cr, eGFR, consider IDC risk/benefit, UO ?0.5mL/kg/hr
pulmonary diseases/airway: may have coexisting restrictive (eg. pectus excavatum) or obstructive airway disease, pre-existing pulm disease prior to transplant, recurrent pneumonias common, Hx prol ventilatory support incr risk postop reap failure. review PFTs & CXR. consider difficult airway risk (eg, if Hx trache or CHD with facial anomalies). Consider opioid-sparing & short-acting analgesics, fully reverse & extubate awake
hepatic disease: eg. from congestive hepatopathy due to pre-transplant HF or due to hepatotoxic meds. Review LFTs incl coats, calculate MELD to determine severity of liver disease
diabetes: steroid-induced, Ax level of control, medication regimen + periop plan, hourly intra-op BGL monitoring, consider first on list & endocrine input
HTN: med management plan
congenital anomalies in pts wth CHD: eg. retrognathia, pectus excavatum
Why may pts with heart transplant be at particular risk of myocardial ischaemia?
cardiac allograft vasculopathy- complication in the late post-transplantation period
What are some airway & ventilation considerations for post-transplant pts?
airway:
oral vs nasal (lower infection risk)
oral may still be bleeding risk (gingival hyperplasia with cyclosporine, chronic anticoagulation, increased vascularity of mucosa due to collaterals in pts with CHD)
Which immunosuppressant risks gingival hyperplasia?
cyclosporine
Which immunosuppressants may lower seizure threshold?
calcineurin inhibitors (cyclosporin, tacrolimus)
If planning to give stress steroid during surgery, does the pt still need to take their am glucocorticoid?
yes
