Intrathoracic organ transplantation has received little attention from the CICM examiners, with the exception of one SAQ (Question 22 from the first paper of 2009) which asks the candidate to "discuss the clinical issues specific to the heart lung transplant" in a patient with pneumonia.
LITFL have an excellent heart transplant overview, with a focus on ICU-level management. Additionally, there is a chapter on this topic in Oh's Manual (Ch.102, pp. 1053) put together by Macdonald and Jansz. This chapter offers some blue boxes full of donation criteria, and a series of protocols detailing the exact doses and timings of the immunomodulators and antimicrobial prophylaxis.
A more detailed summary of complications of combined heart and lung transplantation, focusing on the physiological derangements associated with a long-term transpant, is also available. Specifically, the infectious complications of heart-lung transplantation receive some attention in the Infectious Diseases part of the Required Reading section.
The following brief summary is an attempt to synthesise the most memorable points in Oh's Manual together with the pearls offered by LITFL.
Notes on cardiac transplantation
Survival rates for cardiac transplantation:
- 90% at 1 yr
- 80% at 5 yrs
- 60% at 10 yrs
- Median survival is 11 yrs
- The greatest improvement in survival since the 1980's has affected the first few months following transplant.
Notes on cardiac donation
- Mainly, they are from brain-dead donors (very few are DCD)
- The heart is sensitive to ischaemia, and DCD transplants tend to do poorly
While waiting for a transplant:
- 30-50% of recipents will be waiting while attached to an LVAD or something similar
- Survival rates for a VAD-assisted life are currently around 80% at 2 years.
ICU management of the cardiac transplant patient
- Usually, an uncomplicated case will be extubated within 6-8 hours
- A PA catheter is usually available to monitor PA pressures and pulmonary vascular resistance.
- Bradycardia: The transplanted heart is usually bradycardic for the first 1-2 weeks; ultimately, the rate stabilises at 90-100 bpm, but early pacing is usually required.
- Arrhythmias should not occur - they are uncommon; when arrhythmias are seen, it is usually a prelude to acute rejection.
- Diastolic dysfunction due to reperfusion stunning is a feature of the first 24 hours
- Filling pressures of 10-15mmHg may be required
- If this diastolic dysfunction fails to resolve within a week, it is a sign that acute rejection may be taking place.
- Hypertension occurs for two reasons:
- You have just transplanted a heart into a patient who has adapted to chronic systemic hypotension; the new healthy heart will produce a vigorous increase in arterial blood pressure.
- Cyclosporin drugs (especially tacrolimus) cause hypertension as one of their side effects
- All of this is bad - hypertensive encephalopathy may result from systolic pressures in excess of 140mmHg. GTN or something similar should be used.
Inotropes and vasopressors
- Isoprenaline is used, which appears to be a non-evidence-based tradition
- Adrenaline is co-administered to maintain a MAP over 70mmHg
- Thyroid hormone is for some reason advocated by some authors
Primary graft failure
- Essentially, failure of tre graft to meet circulatory demand
- Defined as hypotension and poor cardiac output in the presence of adequate filling pressures
- Commonest cause of early post-transplant mortality (40% of deaths in the first month)
- VA ECMO, RVAD or LVAD are bridging therapies used to allows some recovery time; however depending on aetiology the graft may never recover.
- Hyperacute rejection usually happens within the first few hours, and is antibody-mediated
- Acute rejection usually happens after the first week, and is T-cell mediated
- Surveillance biopsies are required; occasionally the graft continues to function in a manner which does not allow clinical features of failure to manifest
- High dose methylprednisolone pulse therapy is the treatment of choice
Idiosyncratic features of the transplanted heart
In brief summary:
- Autonomic disconnection:
- No cardiovascular response to hypotension; thus, sepsis or spinal/epidural anaesthesia result in massive hypotension
- Atropine has no effect on heart rate
- Digoxin has no effect on heart rate
- There is no bradycardia in response to cholinergic drugs, eg. neostigmine
- There is no reflex tachycardia in response to GTN
- Adenosine has an exaggerated effect, and one should use 1mg doses
- Inotropes have an exaggerated effect, perhaps with the exception of isoprenaline (?)
- Coronary artery disease is accelerated in these people