Adult Heart Transplantation

Neonatal/Pediatric Heart Transplantation

Position

Supine

⇐

Incision

Median sternotomy

⇐

Special instrumentation

Ascending aortic, SVC, and IVC cannulae

Ascending aortic and right atrial cannulae

Unique considerations

Due to complete excision of the heart, use of a PA catheter is usually not feasible.

Deep hypothermia with circulatory arrest

Antibiotics

Cefazolin 1–2 g iv

Cefazolin 25–50 mg/kg iv

Surgical time

Cross-clamp: 45–60 min
Surgery: 3–4 h

Circulatory arrest: 45–60 min; Cross-clamp:
80–100 minutes
Surgery: 4–6 h

Closing considerations

Temporary AV pacing wires are occasionally placed. A PA catheter may be advanced, especially with concerns about residual pulmonary HTN and donor right heart function. An isoproterenol infusion is started intraop to keep HR = 100–110 and help improve right heart function and ↓ PVR. Inhaled NO may be used to further ↓ PVR.

Temporary ventricular pacing wire is usually placed. Temporary transthoracic left atrial line may be placed. Extensive aortic suture line requires avoidance of postop hypertensive episodes.

EBL

500–1,500 mL

50–100 mL

Postop care

Cardiac ICU: 1–2 d of assisted ventilation;
2–3 d stay.

Pediatric ICU × 1–2 d of assisted ventilation;
4–5 d stay, with attention to pulmonary care.

Mortality

< 5%

⇐

Morbidity

Early acute rejection episodes from 10–21 d: 50%
Infection, particularly pulmonary: 10%
Pulmonary HTN with right heart dysfunction:
< 10%
Dysrhythmias with nodal rhythms: 5%
Bleeding: 2–4%
Hyperacute rejection: Rare (< 1%)
Intracoronary air emboli

⇐
Respiratory problems: 20%
Infection: 10%
Pulmonary vasospasm with right heart dysfunction: < 10%
Bleeding: 2–4%

Pain score

8–10

8–10

Age range

18–75+ yr (average 50–55 yr)

1 d–2 mo (neonatal); 2 mo–18 yr (pediatric)

Male:Female

7:3

1:1

Incidence

2,200/yr (United States)

Rare

Etiology

Cardiomyopathy (50%); CAD with multiple pre
vious infarcts (48%); other (2%)

No apparent correlation with any specific
genetic disorder. Cardiomyopathy (49%); CHD
(42%); other (7%)

Associated conditions

CHF

Other congenital anomalies

Respiratory

The presence of pulmonary HTN and ↑PVR may be disclosed by catheterization. The severity of the abnormality and the responsiveness to specific vasodilators must be determined.
Tests: Right heart catheterization

Cardiovascular

Indicators to consider include: hemodynamic status; LV EF (mortality is rapid in patients with EF < 10% and is worse for patients with EF of 10–20%, as compared with those with EF > 20%); myocardial structure and morphology, symptoms, and functional capacity; neuroendocrine status; serum sodium; and dysrhythmia. Unfortunately, while these measures show trends with mortality, they are not individually strong enough to predict a particular patient's course. Low maximum O₂ consumption (< 10 mL/kg/min) is associated with poor survival. Normal O₂ consumption is 40 mL/kg/min. In practice, however, this measure is too severe, because many patients awaiting heart transplantation have maximum O₂ consumption of 20 mL/kg/min. Dysrhythmia is a major cause of death; unfortunately electrophysiology studies of these patients may not be helpful because dysrhythmia tends to be noninducible. This phenomenon frustrates efforts to select and test antidysrhythmic drug therapy. The effectiveness of past antidysrhythmic therapy should be reviewed.
Tests: ECG; cardiac catheterization; ECHO

Hematologic

Patients with dilated cardiomyopathy or previous cardiac surgery are frequently treated with anticoagulants to reduce the risk of thrombus formation, although the efficacy of this therapy has not been studied. Hepatic dysfunction may result from RV failure and may reduce synthetic function. Mild hepatic dysfunction and chronic anticoagulation may contribute to postop bleeding. The anticoagulant effect of warfarin should be reversed with FFP.
Tests: Hct; PT; PTT; fibrinogen; Plts

Endocrine

Neuroendocrine abnormalities are often present in severe CHF cases. The cardiomyopathy produces low CO → compensatory sympathetic activation and renin-angiotensin activity. The result is excessive vasoconstriction with salt and H₂O retention, which further impair myocardial performance. Markedly worse survival is seen in CHF patients with serum sodium < 130. This may indicate the importance of neuroendocrine pathophysiology or may simply be evidence of the severity of the CHF. It may also simply indicate that patients with more severe CHF are treated with more diuretics. When patients are treated with an angiotensin-converting enzyme inhibitor, such as enalapril, the serum sodium is normalized and survival chances are improved because of the slowing of the progression of CHF, not from alteration in the incidence of sudden death.
Tests: Electrolytes; Cr

Laboratory

Evidence of renal and hepatic dysfunction should be sought by H&P and lab studies. Hypokalemia is generally not treated in view of the K+ in the graft.

Premedication

Although anxious, these patients are usually well informed and psychologically prepared to undergo heart transplantation. They respond well to the reassurance of the preop visit, and pharmacologic premedication usually is not necessary. O₂ therapy should commence prior to transport of the patient to the OR. Reassuring the family of a patient who suffers from rapidly progressive cardiac dysfunction also is valuable. The patient may be at increased risk for pulmonary aspiration of gastric contents because of the unscheduled nature of the surgery and use of oral cyclosporine immediately preop. Ranitidine (50 mg) and metoclopramide (10 mg) may be administered iv, most efficiently accomplished in the OR.

Induction

An arterial line for BP and blood gas monitoring should be inserted, using liberal amounts of local anesthetics before induction. There are rare exceptions to this rule, but the presence of real-time BP monitoring can be critical during induction. If infusion drugs (e.g., dopamine) are necessary before insertion of the CVP catheter, they can be infused temporarily through a separate peripheral iv. In patients who have a ↓ EF, it is often helpful to infuse dopamine 3–10 mcg/kg/min during induction to avoid ↓ HR and ↓ CO. Anesthesia is not induced until the team harvesting the graft reports that the donor heart appears to be normal. The patient is denitrogenated (FiO₂ = 1.0), and cricoid pressure is applied just before induction. Induction agents include fentanyl (5–10 mcg/kg) or sufentanil (1–4 mcg/kg). Etomidate (0.1–0.2 mg/kg) is useful in permitting rapid control of the airway and for assuring lack of patient awareness. Midazolam also may be used. Vecuronium (0.15 mg/kg), pancuronium (0.1 mg/kg), or a combination of these two agents should be administered immediately to permit airway control.
Care must be taken to avoid bradycardia, which often results in low CO in these patients. Immediate control of the airway is crucial, as hypercarbia and hypoxia must be avoided. The patient can be expected to have a low CO, resulting in a delayed induction of anesthesia, which must be anticipated to avoid anesthetic overdosage. Low CO and a volume-contracted condition make the patient initially very sensitive to anesthetics. Hypotension should be treated promptly with inotropes (bolus and/or infusion). High preload is often necessary, and iv fluid may be administered cautiously to compensate for the vasodilating effect of anesthetic-mediated sympatholysis. Fluid boluses may be poorly tolerated in patients with diminished contractility.
Patient should be ventilated by mask and cricoid pressure released only after the airway has been secured with a cuffed ETT. The usual aids for managing the unexpectedly difficult airway should be readily available. Antibiotics are administered, and additional monitors (urinary catheter with thermistor, nasopharyngeal temperature probe, TEE, or esophageal stethoscope) are set up. If there is a delay in the anticipated arrival of the graft, the recipient should be covered and kept warm and skin prep should be delayed. Additional narcotics should be administered only in immediate anticipation of the commencement of surgery.

Maintenance

Typical cumulative anesthetic doses for the entire intraop course are: fentanyl 20–50 mcg/kg or sufentanil 10–15 mcg/kg; midazolam 0.2 mg/kg; vecuronium 0.3 mg/kg or pancuronium 0.2 mg/kg; scopolamine 0.07 mg/kg.

Termination of CPB

Junctional rhythm is common in the denervated transplanted heart. Isoproterenol 10–75 ng/kg/min or epinephrine 50–105 ng/kg/min may be used to achieve a HR of 100–120 bpm. Isoproterenol is also useful in providing inotropic support and pulmonary vasodilation (see below). Atropine and neostigmine do not affect HR. HTN does not produce reflex bradycardia. The graft atrium produces normally conducted P-waves. The graft-conductive tissue contains adrenergic receptors and responds normally to norepinephrine, epinephrine, and isoproterenol.
Inotropic support with dopamine (2–10 mcg/kg/min), isoproterenol (10–150 ng/kg/min), and epinephrine (20–100 ng/kg/min) may be necessary, especially if pulmonary HTN promotes RV failure. Inhaled NO (20–40ppm) may provide selective pulmonary vasodilation. A PA catheter may be helpful in guiding the use of inotropes and vasodilators.
After termination of CPB, TEE may be of particular value in assessing RV dysfunction, estimating PA pressures and guiding appropriate fluid therapy, pharmacologic support, and mechanical support as necessary. RV failure may be produced by the presence of air in the RCA. Visual inspection may demonstrate this problem, and one should wait for the passage of the air and the resolution of ischemia before terminating CPB.
SNP (0.2–2.0 mcg/kg/min) is used for afterload reduction. NO, prostaglandin E₁ (PGE₁) (20–100 ng/kg/min), and NTG (0.2–2.0 mcg/kg/min) may be used for pulmonary vasodilation, especially if a preop catheterization study demonstrates responsiveness of the pulmonary circulation. Isoproterenol infusion (10–100 ng/kg/min) may provide appropriate pulmonary vasodilation, chronotropy, and inotropy. IV fluid and vasodilators must be given with particular care, as the flow produced by the denervated heart is quite sensitive to preload.

Postbypass hemorrhage

Postbypass bleeding is a common problem brought on by the preop use of anticoagulants, the depressed synthetic function of the liver in chronic heart failure, and the trauma of CPB. Following administration of protamine, infusion of Plts, FFP, and RBCs may be necessary. Cryoprecipitate is needed occasionally, especially for patients with previous chest surgery. The use of aprotinin, epsilon amino caproic acid (EACA), or tranexamic acid may be appropriate in some cases.

Immuno- suppression

Methylprednisolone 500 mg is given after bypass is terminated. Daclizumab 1 mg/kg is also administered after administration of protamine, and hemostasis has been secured.

Diuresis

There may be little urine production, especially if patient received high-dose diuretics preop. Cyclosporine may exacerbate renal dysfunction. Mannitol and furosemide may be needed to induce diuresis.

Transport

A Jackson-Rees system is used in transporting the patient to the ICU.

Blood and fluid requirements

Possible severe bleeding
IV: 14–16 ga × 1–2
NS/LR @ 4–6 mL/kg/h

Bleeding is often a problem after termination of
CPB. A second iv catheter is inserted in patients
with previous chest surgery.

Monitoring

Standard monitors (see p. B-1).
Arterial line
CVP/PA catheter
UO

Although it may be helpful to have a triple-lumen CVP line before induction for preload monitoring and infusion of potent infusion drugs, it is not essential. This line is usually inserted after the patient is intubated to avoid patient dyspnea and discomfort. A PA catheter is usually not inserted before bypass since it must be removed during surgery. An 8.5-Fr introducer is used in anticipation that a PA catheter may be necessary to manage right heart failure following the transplantation. In some institutions (not Stanford), the left IJ vein is the preferred site of cannulation, which leaves the right IJ unscarred for repeated postop endomyocardial biopsy of the transplanted heart.

TEE

TEE is used to optimize fluid therapy, inotropic agents, vasodilators, and chronotropic agents.

Positioning

[check mark] and pad pressure points.
[check mark] eyes.
Arms padded at sides
Chest roll

Complications

RV dysfunction
Pulmonary HTN

RV failure may occur in patients with pulmonary HTN and high RV afterload (see pulmonary HTN, below).
Maneuvers which exacerbate pulmonary HTN should be avoided. These include hypoxia, hypercarbia, acidosis, and extremes of lung volume. Inhaled NO can be used to treat pulmonary HTN (20–40 ppm inspired concentration); however, it must be used with caution in patients with severe heart failure. Efforts to treat pulmonary HTN with vasodilator therapy may be complicated by impaired V/Q matching with hypoxemia and by systemic ↓ BP producing poor coronary perfusion and RV ischemia. Inotropic support of the RV may be necessary. Isoproterenol infusion (10–150 ng/kg/min) is attractive because it combines inotropy, pulmonary vasodilation, and chronotropy.

Oliguria
Drug side effects:

· Cyclosporine: HTN, nephrotoxicity, hepatotox
icity

· Corticosteroids: glucose intoler
ance, HTN, obesity, hyperlipi
demia, aseptic necrosis of hip,
bowel perforation, infection

Preexisting impairment may → chronic ↓ UO state. Other renal problems may be related to cyclosporine toxicity, diuretic toxicity, or CPB. Rx by optimizing hemodynamics. Consider reduction or elimination of nephrotoxins and continuing use of diuretics. Cyclosporine nephrotoxicity occurs in most patients. A functional toxicity with ↓ GFR occurs at low dose and is reversible. Tubular toxicity with morphologic changes occurs at high doses and is generally clinically unimportant and reversible. The most serious damage is vascular interstitial toxicity, which occurs over months at high doses and is not reversible.

Pain management

PCA (see p. C-3) after weaning
from mechanical ventilation.

Tests

Cr
Hct

Heart/lung Transplantation

Single-Lung Transplantation

Bilateral-Lung Transplantation

Position

Supine

Lateral thoracotomy

Supine

Incision

Median sternotomy, usual; bilateral anterior thoraco tomy, occasionally

Posterolateral thoracotomy

Transsternal bilateral
thoracotomy

Special instrumentation

Ascending aortic, SVC, and IVC cannulae

Occasional need for BB to be inserted through the operative field.

± Aortic, SVC, and IVC cannulation; occasional need for BB.

Unique considerations

CPB. If recipient has had previous thoracotomies, mediastinal collaterals may cause troublesome bleeding. Some patients with cystic fibrosis have severe bilateral
scarring, requiring extensive dissection to remove the reipient lung.

± CPB. Patient may become severely hypoxic or hypercarbic during OLV, requiring CPB. During right thoracotomy, cannulation can be performed through the thorax, but left thoracotomy may require femoral artery and vein cannulation.

CPB. Thoracotomy usually is performed on left side first, with implantation of lung on this side, followed by completion of right side thoracotomy and right-lung transplantation. If patient becomes unstable, cannulation in the thorax is usually possible to facilitate transplantation.

Antibiotics

Continue specific antibiotic regime. Coverage for pseudomonas is suggested in patients with cystic fibrosis.

Cefazolin 2 g iv then 1g q 4 h

⇐ With appropriate coverage for pseudomonas in patients with cystic fibrosis.

Surgical time

4–5 h

2–3 h

5–6 h

Closing considerations

Temporary pacing wire applied and isoproterenol infusion is usually started intraop to keep HR between 100–110, as with a cardiac transplant.

Ventilation with as low an FiO₂ as possible to maintain a PO₂ > 90. Minimize iv fluids.

⇐

EBL

500–2,000 mL

< 500 mL (more if CPB is used)

500–2,000 mL

Postop care

Cardiac ICU: 3–7 d; 1–2 d assisted ventilation

⇐

⇐

Mortality

10–15%

10%

10–15%

Morbidity

Early acute rejection episodes from 10–21 d: 75%

—

—

Infection, particularly pulmonary: 30–40%

⇐

⇐

Pulmonary interstitial edema: 20%

Bleeding: 2–4%
Bronchial leak or stenosis:

⇐

2–4%

⇐

Return for bleeding: 4–6%
Hyperacute rejection: Rare

Pain score

8–10

8–10

8–10

Heart/lung
Transplantation

Single-Lung
Transplantation

Bilateral-Lung
Transplantation

Age range

3 mo–55 yr (average 30–40 yr)

1–65 yr

⇐

Male:Female

1:1

⇐

⇐

Incidence

~30/yr (United States)
200/yr (worldwide)

600/yr (United States)
1,000/yr (worldwide)

800/yr (United States)
1,200/yr (worldwide)

Etiology

Eisenmenger's syndrome; CHD; cystic fibrosis; pulmonary HTN; other lung diseases

Acquired chronic lung disease; pulmonary HTN

Cystic fibrosis; interstitial fibrosis; emphysema

Associated conditions

Severe cyanosis and polycythemia; diabetes in patients with cystic fibrosis; sinus infections in patients with cystic fibrosis

Right heart dysfunction; pulmonary valve insufficiency and tricuspid valve insufficiency

Diabetes mellitus; sinus infections in patients with cystic fibrosis

Respiratory

Patients with severe pulmonary HTN (80/50 mmHg) have enlarged PAs. Vocal cord dysfunction (Sx: hoarseness, inability to phonate “e”) may occur when the left recurrent laryngeal nerve is stretched by an enlarged PA, making these patients at increased risk for pulmonary aspiration. Appropriate precautions to avoid aspiration should be taken (see Induction, below).
Tests: ABG; cardiac catheterization

Cardiovascular

Hx of recent exacerbation of symptoms should be sought and cardiac catheterization data interpreted in light of interval changes. The severity of pulmonary HTN and the responsiveness to specific vasodilators during catheterization should be reviewed.
Tests: ECG; cardiac catheterization; ECHO

Neurological

R → L intracardiac shunting may be present in patients with pulmonary HTN, and Hx of embolic episodes should be sought. Extra care should be used to avoid injection of even small quantities of intravenous air.

Hematologic

The medication schedule should be verified with particular attention to the recent use of anticoagulants.
Tests: Hct; PTT; PT (special tubes required if severe polycythemia present 2° ↓ plasma volume); Plt count; fibrinogen

Laboratory

Evidence of renal and hepatic dysfunction should be sought by H&P and lab studies. Hypokalemia is generally not treated because the heart/lung graft is preserved with K+ and implantation will reverse hypokalemia.

Premedication

Although anxious, these patients are usually well informed and psychologically prepared. They respond well to the reassurance of the preop visit, and pharmacologic premedication usually is not necessary. O₂therapy should commence prior to transport of patient to the OR. Patient may be at increased risk for pulmonary aspiration of gastric contents because of the unscheduled nature of the surgery, the use of oral cyclosporine immediately preop and the presence of recurrent laryngeal nerve damage. Ranitidine (50 mg) and metoclopramide (10–20 mg) may be administered iv preop.

Induction

In the OR, the patient should be placed on the operating table and O₂ and noninvasive monitors applied. An arterial line for BP and blood gas monitoring should be inserted, using liberal amounts of local anesthetics before induction. There are rare exceptions to this rule, but the presence of real-time BP monitoring can be critical during induction. A patient who is dyspneic in the supine position may be treated by raising the back of the table. Cricoid pressure must be used when the patient is at risk for aspiration of gastric contents. A major goal of anesthetic induction is the avoidance of further increases in PVR by guarding against respiratory acidosis, hypoxia, N₂O, light anesthesia, and extremes of lung volume. When hemodynamically tolerated, fentanyl (5–10 mcg/kg) is useful in blunting the pulmonary vascular response to intubation.
Etomidate (0.1–0.2 mg/kg) may be used when hypotension limits administration of narcotics. Vecuronium (0.15 mg/kg), pancuronium (0.1 mg/kg), or a combination of the two, should be administered early to permit rapid airway control. Midazolam and scopolamine produce amnesia. N₂O is not used because it exacerbates pulmonary HTN, reduces FiO₂, and expands intravascular air bubbles. Patient should be ventilated by mask, and cricoid pressure released only after the airway has been secured with a cuffed ETT. Excessive pressure of the cuff on the trachea should be avoided. An ETT of internal diameter of 8.0 mm will facilitate FOB postop.

Maintenance

Typical total anesthetic doses for the entire intraop course are: fentanyl 10–50 mcg/kg or sufentanil 10–15 mcg/kg; midazolam 0.2 mg/kg; vecuronium 0.3 mg/kg or pancuronium 0.2 mg/kg; scopolamine 0.07 mg/kg.

Termination of CPB

After tracheal anastomosis is complete, lungs are ventilated with FiO₂ = 0.21 at 5 breaths/min and a TV of 6 mL/kg. When bladder temperature reaches 36°C, ventilation is increased to 10 breaths/min and TV of 12 mL/kg. TV should be adjusted to eliminate atelectasis and to achieve a peak inflation pressure of 25–30 cmH₂O with the chest open. The FiO₂ is increased to 0.4 and may be altered in response to pulse oximetry and blood gas data. FiO₂ is limited in the hope of curtailing free radical injury. PEEP may be used to enhance oxygenation and is adjusted with an appreciation of the effect of lung volume on PVR. Hypoxemia must be avoided. Hyperkalemia may be treated with Ca++ (e.g., 3–5 mL 10% CaCl q 30 min), glucose (50 g), insulin (10 U), and diuresis.
Junctional rhythm is common in the denervated transplanted heart. Epinephrine (50–150 ng/kg/min) or isoproterenol (10–75 ng/kg/min) is used to achieve a HR of 100–120. When sinus rhythm is achieved, it is common to see two P-waves if a biatrial anastomosis has been used. The residual atrial tissue produces nonconducting P-waves. Responses mediated by vagal tone will be seen in the rate of the original atrial tissue and have no clinical importance beyond the ease with which the ECG is interpreted.
In the denervated heart, atropine and neostigmine will not affect HR, and HTN will not produce reflex bradycardia. The graft atrium produces normally conducted P-waves. The transplanted heart contains adrenergic receptors and responds normally to norepinephrine, epinephrine, and isoproterenol.
The CO of the denervated heart is quite sensitive to preload; thus, iv fluid and vasodilators must be given with particular care. SNP is used for afterload reduction. TEE may be of particular value in assessing RV dysfunction and guiding appropriate fluid therapy, pharmacologic support, and mechanical support as necessary. NO, PGE₁ (20–100 ng/kg/min), isoproterenol, and NTG (0.2–2.0 mcg/kg/min) also may be used for pulmonary vasodilation. Inotropic support with dopamine (2–10 mcg/kg/min), isoproterenol, and epinephrine (20–100 ng/kg/min) may be necessary, especially if pulmonary HTN and RV failure occur.

Immuno- suppression

Methylprednisolone 500 mg iv is given after bypass is terminated.

Diuresis

There may be little urine production, especially if patient received high-dose diuretics preop. Cyclosporine may exacerbate renal dysfunction. Mannitol and furosemide may be needed to induce diuresis.

Transport

A sterile, disposable Jackson-Rees system is used in transporting the patient to the ICU.

Blood and fluid requirements

Anticipate large blood loss.
IV: 14–16 ga × 2

Bleeding is often a major problem after termination of CPB. Patients with intracardiac defects are at increased risk for cerebral embolic events. Care must be taken to remove all air bubbles from intravascular lines.

Control of blood loss

Postbypass bleeding is a common problem.

Postbypass bleeding is exacerbated by preop use of anticoagulants, depressed synthetic liver function, trauma of CPB, and/or previous chest therapy.

Coagulation therapy necessary.

Coagulation therapy may include: protamine (30 mg/kg); Plts; FFP; RBCs; EACA (300 mg/kg); DDAVP; aprotinin (500,000 U/h after loading dose).

Possible severe bleeding

Severe bleeding prompts further therapy: cryoprecipitate, factor IX concentrate, Feiba VH (factor 8 inhibitor bypassing activity), and/or recombinant factor 7a.

Monitoring

Standard monitors (see p. B-1).
Arterial line

CVP/PA catheter
UO

Typically, invasive monitors are placed prior to induction; however, if patient is very dyspneic in the supine position, it may be advantageous to insert the CVP catheter following anesthetic induction. An introducer permits the rapid insertion of a PA catheter when necessary. In some centers (not Stanford) the left IJ vein is the preferred site of cannulation, leaving the right IJ unscarred for repeated endomyocardial biopsies of the transplanted heart.

TEE

TEE is used to optimize volume status (LV + RV size), inotropic agents (LV + RV contractility), vasodilators, and chronotropic agents.

Complications

Oliguria
Pulmonary edema
RV dysfunction

Diuresis may be induced with mannitol and furosemide.
Given the lack of lymphatic drainage in the transplanted lung, pulmonary edema may occur. Diuresis and restriction of iv fluid may be required.
RV failure may occur in patients with pulmonary HTN and high RV afterload (see pulmonary HTN Rx, below).
Pulmonary HTN
Rejection
Infection
Drug side effects:

· Cyclosporine: HTN, nephrotoxicity, hepatotoxicity

· Corticosteroids: glucose intolerance, HTN, obesity, hyperlipidemia, aseptic necrosis of hip, bowel perforation, infection

· Azathioprine: anemia, thrombocytopenia, leukopenia, hepatotoxicity

Maneuvers which exacerbate pulmonary HTN should be avoided. These include hypoxia, hypercarbia, acidosis, and extremes of lung volume. NO can be used to treat pulmonary HTN (0.1–100 parts per million inspired concentration); however, it must be used with caution in patients with severe heart failure. Efforts to treat pulmonary HTN with vasodilator therapy may be complicated by impaired V/Q matching with hypoxemia and by systemic hypotension, producing poor right coronary perfusion and RV ischemia. Inotropic support of the RV may be necessary. Isoproterenol is attractive because it combines inotropy, pulmonary vasodilation, and chronotropy.
Monitor rejection Sx with transvenous endomyocardial biopsy and transbronchial biopsy.
Cyclosporine nephrotoxicity occurs in most patients. A functional toxicity with reduced GFR occurs at low dose and is reversible. Tubular toxicity with morphologic changes occurs at high doses and generally is clinically unimportant and reversible. The most serious damage is vascular interstitial toxicity, which occurs over months at high doses and is not reversible.

Pain management

PCA (see p. C-3).

Respiratory

Assess the patient's ability to undergo OLV by review of the V/Q scan. If little perfusion of the nonoperative lung is present, anticipate the need for CPB. The extent of the restrictive lung disease and diffusion abnormality must be assessed preop. For example, room-air PaO₂ < 45 mmHg predicts the need for CPB.
Tests: PFT; V/Q scan; ABG

Airway

Patients with severe pulmonary HTN (80/50 mmHg) have enlarged pulmonary arteries. Vocal cord dysfunction (Sx: hoarseness, inability to phonate “e”) may occur when the left recurrent laryngeal nerve is stretched by an enlarged PA, making these patients at increased risk for pulmonary aspiration; therefore, appropriate precautions to avoid aspiration should be taken (see Induction, below).

Cardiovascular

Evidence of RV dysfunction with tricuspid regurgitation should be sought by physical exam, ECHO, and cardiac catheterization. RV ejection fraction (EF) may be estimated with radionuclide ventriculography (normal EF = > 50%). Pulmonary HTN is considered to be severe and may produce RV failure when pressure is > 2/3 of systemic arterial pressure. Note response to specific vasodilators recorded during catheterization.
Tests: Preview cardiac catheterization data; ECG; mean PAP > 40 mmHg and PVR > 5 mmHg/min/L may predict the need for partial CPB.

Neurological

R→L intracardiac shunting may be present in patients with pulmonary HTN, and Hx of embolic episodes should be sought. Extra care should be used to avoid injection of even small quantities of intravenous air.

Musculoskeletal

Chronic cachexia precludes the procedure.

Hematologic

Polycythemia 2° chronic hypoxemia is common. Autologous blood is collected as CPB is initiated.
Tests: Hct; coagulation studies require special blood tubes to correct for low plasma volume in patients with severe polycythemia.

Laboratory

Other tests as indicated from H&P.

Premedication

Patients awaiting lung transplantation are generally well informed about the planned perioperative course. These patients respond well to the reassurance of the preop visit, and pharmacologic premedication usually is not necessary. O₂ therapy, with the usual home O₂ regimen, should commence prior to transport to the OR. Patient may be at ↑ risk for pulmonary aspiration of gastric contents because of the unscheduled nature of the surgery, the use of oral cyclosporin immediately before surgery, and the presence of recurrent laryngeal nerve damage. Ranitidine (50 mg) and metoclopramide (10–20 mg) may be administered iv before surgery.

Induction

An arterial line for BP and blood gas monitoring should be inserted, using liberal amounts of local anesthetics before induction. There are rare exceptions to this rule, but the presence of real-time BP monitoring can be critical during induction. Typically, fentanyl 5–10 mcg/kg (incremental doses) after invasive monitors placed, ± etomidate 0.1–0.2 mg/kg when rapid control of the airway is desirable; vecuronium 0.15 mg/kg or pancuronium 0.1 mg/kg (avoid succinylcholine 2° ↓ HR); midazolam 0.1 mg/kg or scopolamine 0.005 mg/kg for amnesia. Cricoid pressure must be used when the patient is at risk for aspiration because of the unscheduled nature of the surgery, use of preop oral cyclosporin, and possible vocal cord dysfunction associated with stretch injury of the recurrent laryngeal nerve. Avoid further increases in PVR by guarding against hypoxemia, acidosis, hypercarbia, light anesthesia, and extremes of lung volume.

Maintenance

Typically, narcotic/O₂/air/± isoflurane (in absence of hypoxemia and right heart failure). Typical total anesthetic doses for the entire intraop course: fentanyl 20–50 mcg/kg or sufentanil 10–15 mcg/kg, midazolam 0.2 mg/kg, vecuronium 0.3 mg/kg, or pancuronium 0.2 mg/kg, scopolamine 0.07 mg/kg.

Emergence

Before closure of the chest, lungs are inflated to 35 cmH₂O to reinflate atelectatic areas and check adequacy of bronchial closure. At the conclusion of surgery, both lumens of the DLT should be suctioned and the tube replaced with a single-lumen 8.0 mm ETT. The patient is transported to the ICU intubated and ventilated.

Blood and fluid requirements

IV: 14 or 16 ga × 1–2
NS/LR @ 4 mL/kg/h

Patients with intracardiac defects are at increased risk for cerebral embolic events; take care to remove all air bubbles from intravascular lines.

Monitoring

Standard monitors (see p. B-1).
Arterial line
PA catheter
Urinary catheter with thermistor
TEE

ECG leads should be covered with tape to insure that electrical contact is not degraded by prep solution or blood. Mixed venous oximetry may be desirable during OLV, and with partial CPB. Be careful of air embolization during catheter insertion. Patients who are profoundly dyspneic (→ high negative intrathoracic pressure) are at high risk for VAE; consider inserting the catheter after GA and IPPV have been instituted. Oxygenation must be watched closely. Blood gases are sampled at 10-min intervals.
RV EF measurement may be useful for evaluating RV function (normal EF = 0.5–0.7).

OLV

DLT: 41 Fr (men); 39 Fr (women)
Use large TV (12–15 mL/kg) during regular and OLV.
Frequent suctioning

A DLT is inserted in the left mainstem bronchus to permit surgical access. FOB is used to verify proper tube placement. Positioning of the bronchial cuff in the proximal left mainstem bronchus does not interfere with surgical access to the bronchus. The position of the DLT should be verified after the patient is moved to the lateral position. Finally, verify ventilation and proper functioning of the tube, then eliminate volatile anesthetic or vasodilators, which may blunt hypoxic pulmonary vasoconstriction. Apply O₂ with CPAP at 5 cmH₂O to the nondependent lung. Further adjustment of CPAP may enhance oxygenation. The nondependent lung may be reinflated with O₂, if necessary, to achieve adequate oxygenation. If adequate oxygenation cannot be achieved, CPB should be initiated.
Frequent suctioning is necessary in patients with tenacious secretions.

PA clamping

Improve V/Q mismatch.
Improve oxygenation.
PAP ↑↑→ RV failure

Clamping of the PA will improve V/Q mismatch and oxygenation; however, severe pulmonary HTN and RV failure may develop. Vasodilators, such as NTG (0.2–2 mcg/kg/min), SNP (0.2–10 mcg/kg/min), PGE₁ (20–100 ng/kg/min) or inhaled NO (20–40 ppm) should be used to treat pulmonary
HTN and ↓ RV afterload; however, care must be taken to avoid systemic hypotension. Inotropic support for the RV may be necessary (dopamine [2–10 mcg/kg/min] or epinephrine [20–100 ng/kg/min]). The right atrial pressure should be monitored for evidence of tricuspid regurgitation associated with RV dilation.

PA unclamping

PIP: 20–25 cmH₂O
O₂ sat: 95–100%
PEEP: 5–10 mmHg

Temporary unclamping of the PA may be necessary to allow further pharmacologic therapy. If RV failure cannot be controlled pharmacologically, CPB should be initiated. The PA should not be unclamped until ventilation is possible to the transplanted lung. Perfusion without oxygenation of the transplanted lung would produce profound shunt and hypoxemia. TV should be adjusted to eliminate atelectasis and to achieve a PIP of 20–25 cmH₂O with the chest open. The FiO₂ (0.35) is limited in the hope of curtailing free radical injury. PEEP may be used to enhance oxygenation.

Positioning

For single-lung:

· Supine to lateral decubitus

· Axillary roll

· Airplane splint

· Avoid arm hyperextension
(> 90°).

For double-lung:

· Supine with arms above head for
bilateral subcostal incision

[check mark] and pad pressure points.
[check mark] eyes.

Verify correct position of DLT or BB after moving patient to the lateral position.
Difficult access to airway after patient positioned.
*NB: potential for kinking of iv and arterial lines

Complications

Pulmonary edema
Infection: bacterial, viral, fungal, or protozoan
Side effects of immunosuppressive agents:

· Corticosteroids: HTN, osteoporosis, glucose intolerance, hyperlipidemia

· Azathioprine: anemia, thrombocytopenia, leukopenia

Given the lack of lymphatic drainage in the transplanted lung, pulmonary edema may occur. Diuresis and restriction of iv fluid may be required. Mannitol and furosemide can be used to induce diuresis.
Immunosuppression drugs typically include: tacrolimus, myophenolate mofetil, and corticosteroids. Early induction therapy with a cytolytic agent (e.g. antithymocyte globulin) may be used.

Pain management

Epidural narcotics (see p. C-2)
Parenteral narcotics (see p. C-2)

Postop analgesia may be provided by infusion of narcotics through an epidural catheter. If CPB is used, the insertion of the epidural catheter should be delayed until normal coagulation function is documented in the ICU.