**7. Hemodynamic management**

Hemodynamic stability, after heart transplant, may be impaired by several pathophysiological processes, including autonomic denervation, with subsequent chronotropic and inotropic failure, ischemia reperfusion injury, metabolic acidosis, and volume depletion. To support such effects, several endpoints must be taken into account:

## **7.1. Intravascular volume optimization**

A goal-directed therapy is the ideal way to ensure adequate fluid filling. It means using the above-mentioned hemodynamic parameters coming from invasive monitoring and from echocardiographic evaluation, to be guided in the fluid replacement. Once the need of fluids is clear, the physician should decide the most ideal fluid in order to avoid peripheral organ oncotic damage (i.e., hyperoncotic kidney failure from hydroxyethyl starches [15]); hyperchloremic hyperkalemic acidosis, which can impact itself on kidney function; and fluid overload into the interstitial space. Crystalloids have a less oncotic power than colloids; however, albumin can cross the pulmonary capillary membrane, if damaged, and anyway it can recirculate through the pulmonary barrier 24 hours from the administration: then balanced crystalloids and balanced colloids (albumin solution at 5 or 20%) should be given at the right per kilo amount and the fluid responsiveness should be tested while they are given.

#### **7.2. Narrow monitoring of hemodynamic parameters**

During the recovery period (approximately 7–14 days), a narrow monitoring of hemodynamic and vital parameters is mandatory: IBP, CI, CO, ISVRI, IPVR, PAPs, HR, SvO2 , LAP/PCWP, TPG, SpO2 , ECG, body temperature, urine output, and lactate levels.

Target values are: CVP ≤ 12 mmHg, MAP > 65 mmHg, LAP 8–12 mmHg, SvO<sup>2</sup> over 65%, HR about 100–110 bpm, urine output > 1.5 ml/kg, and lactate < 2 mmol/L.

#### **7.3. Pharmacological support**

treated with low-dose isoprenaline (0.01–0.04 mcg/kg/min), adrenaline (0.01–0.04 mcg/kg/ min), and/or temporary atrial pacing, in order to ensure a heart rate about 100–110 bpm. In case of severe AV block, a sequential pacing is required. Anyway, if the patient is still pacing dependent after 2 weeks from the operation, implantation of a permanent pace maker should be considered. Then, you can proceed to request chest X-ray to check the lungs, endotracheal and nasogastric tube position, chest drains, and intravascular devices (CVP line, PAC, and pacing wires) and send for laboratory tests including standard coagulation, renal and liver function, platelets, red blood cell and white blood cell counts, troponin I, CK, albumin, viral markers, thyroid markers, and glycaemia. Blood samples should be sent for good practice also for coagulation tests (ROTEM or TEG) in case of excessive bleeding. A plan for immunosuppressive therapy (methylprednisolone, thymoglobulins, etc.) must be provided in collaboration with specialist immunologist and cardiologist. Antibiotic therapy must be tailored

Hemodynamic stability, after heart transplant, may be impaired by several pathophysiological processes, including autonomic denervation, with subsequent chronotropic and inotropic failure, ischemia reperfusion injury, metabolic acidosis, and volume depletion. To support

A goal-directed therapy is the ideal way to ensure adequate fluid filling. It means using the above-mentioned hemodynamic parameters coming from invasive monitoring and from echocardiographic evaluation, to be guided in the fluid replacement. Once the need of fluids is clear, the physician should decide the most ideal fluid in order to avoid peripheral organ oncotic damage (i.e., hyperoncotic kidney failure from hydroxyethyl starches [15]); hyperchloremic hyperkalemic acidosis, which can impact itself on kidney function; and fluid overload into the interstitial space. Crystalloids have a less oncotic power than colloids; however, albumin can cross the pulmonary capillary membrane, if damaged, and anyway it can recirculate through the pulmonary barrier 24 hours from the administration: then balanced crystalloids and balanced colloids (albumin solution at 5 or 20%) should be given at the right per kilo amount and the fluid responsiveness should be tested

During the recovery period (approximately 7–14 days), a narrow monitoring of hemodynamic

, LAP/PCWP,

over 65%, HR

and vital parameters is mandatory: IBP, CI, CO, ISVRI, IPVR, PAPs, HR, SvO2

, ECG, body temperature, urine output, and lactate levels.

Target values are: CVP ≤ 12 mmHg, MAP > 65 mmHg, LAP 8–12 mmHg, SvO<sup>2</sup>

about 100–110 bpm, urine output > 1.5 ml/kg, and lactate < 2 mmol/L.

on the background history of donor and/or recipient.

such effects, several endpoints must be taken into account:

**7.2. Narrow monitoring of hemodynamic parameters**

**7. Hemodynamic management**

142 Heart Transplantation

**7.1. Intravascular volume optimization**

while they are given.

TPG, SpO2

The goal is to ensure adequate CO, avoiding excessive increase of cardiac preload and afterload, while maintaining adequate heart rate. Chronotropic support is achieved through low-moderate dose of isoprenaline or by atrial-sequential external pacing. Inotropic effect is achieved through moderate-high dose of adrenaline and, when necessary, with phosphodiesterase inhibitors as milrinone that also decreases peripheral vascular resistances. Other pharmacological tools that are aimed to control arterial ventricle coupling are nitroglycerin and sodium nitroprusside, very helpful to decrease the afterload of the left ventricle and increase cardiac output, when used together with an inotropic drug. In case of preexistent pulmonary hypertension, inhalation of nitric oxide and imbrication with sildenafil can help to reduce pulmonary vascular resistances [14]. In the further postoperative course, addition of an upstream therapy including ace inhibitors, b-blockers, or calcium antagonists may be helpful as cardiac protection.

### **7.4. Support the right ventricle of the donor heart**

The donor heart, particularly the right ventricle, in case of preexisting precapillary or postcapillary pulmonary hypertension, has to fight with high afterload [**Table 6**]. The preexisting conditions may be impaired in case of coexisting hypoxia or hypercapnia, prolonged extracorporeal circulation, and donor ischemia with consequent ischemia-reperfusion injury, blood transfusion, and protamine administration. Right ventricular failure may be challenging and really impacts on the overall survival of transplanted patients [18].

Early PA pressure monitoring at the time of CPB weaning is fundamental and has to be continued in the early postoperative period. The first aim in hemodynamic management of the graft is to offload the right ventricle, decreasing PA pressures and pulmonary vascular resistances while ensuring an adequate RV contractility. Inhaled nitric oxide at 20–40 ppm is a rapid onset tool to decrease PA pressures. It seems to improve early clinical outcomes in heart transplanted patients, but literature is still lacking in terms of overall survival [9].

This is the reason why it is often used preventively during weaning from the CPB.Alternatively, the prostacyclin analog iloprost (6 × 5–10 mcg) can be given.

After the very early postoperative period, inhaled nitric oxide can be substituted by the phosphodiesterase-5 inhibitor sildenafil at the dosage of 20 mg × 3/die via NG tube with very small effects on the systemic pressures, avoiding also the rebound phenomena coming from the discontinuation of inhaled nitric oxide therapy. Sildenafil has also been shown to decrease PA pressures during inhalation of nitric oxide, since they seem to activate different regulatory mechanisms of the vascular tone [19, 20]. Inotropic support of the RV should be guaranteed by moderate-high dose of adrenaline (0.05–0.1 mcg/kg/min) or low-moderate doses of phosphodiesterase inhibitors as milrinone (0.2–0.3 mcg/kg/min).

Clearly, while supporting the right ventricle, we need to ensure adequate oxygenation, avoid hypercapnia, maintain adequate lung recruitment by PEEP (not over 6 cmH<sup>2</sup> O), and guarantee a negative fluid balance in order to reduce the preload and optimize the afterload [**Table 6**]. If all these maneuvers are not sufficient, we have to consider a temporary mechanical right ventricle support via peripheral VA-ECMO.


necessary in a long-term postoperative period, the change is made to intermittent dialysis

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At first, we may exclude significant pericardial collection, assess left ventricle diastolic function of the new performing heart, related to its stiffness and hypertrophy, and think about which wedge pressure we are expected to find [21]. If the systolic function of the new heart is failing, we should exclude an acute graft rejection. Regarding the right ventricle, we must know the recipient preoperative pulmonary vascular resistances, if pre- or postcapillary pulmonary hypertension persists and if it is reversible with phosphodiesterase inhibitors.

RV dysfunction is identified early with a dilation of the right chambers, alteration of interven-

A patient undergoing heart transplant should remain under mechanical ventilation until hemodynamic stability is ensured, lactate levels are stable, and immunosuppressive therapy is started. To protect the lungs, we have to limit peak pressures and use low tidal volumes

However, disadvantages coming from permissive hypercapnia on the pulmonary vascular resistances and right ventricle afterload, myocardial function, and renal blood flow loads must be taken into account [16]. As a consequence, there are no universal evidences, but the choice must be tailored for the patient. The only certainty is we must avoid hypercapnia,

During mechanical ventilation, inhaled nitric oxide can be administered in order to reduce right PA pressures, pulmonary vascular resistances, and then right ventricle afterload, especially in the first 24 hours from CPB weaning at the maximum dosage of 20–40 ppm [17, 18]. Once mechanical ventilation is discontinued, inhaled nitric oxide can be substituted by iv or oral pulmonary vasodilators as sildenafil. The weaning criteria do not differ from those used in normal cardiosurgical patients, and the goal is the same: maintain adequate analgesia and sedation levels and wean the patient from the mechanical ventilation as soon as possible. If this is not possible, due to unstable hemodynamics, high inotropic score, respiratory failure, or neurological issues, a percutaneous dilatation tracheostomy will be packaged without fur-

Once the patient is awake and self-breathing and the LAP line is removed (generally

Early feeding is important. It is initially given via NG tube (25–30 kcal/kg/day) and then self-

24–48 hours from surgery), the patient will need physiotherapy and mobilization.

O).

O and keep peak pressure under 35–40 cmH2

O.

**7.6. Consider echocardiography as a main tool, together with PAC, to guide** 

tricular septum movement, and appearance of tricuspid valve insufficiency.

**hemodynamic management, inotropic support, and fluid challenge**

(three times weekly).

**8. Respiratory weaning**

hypoxia, and PEEP over 10 cmH<sup>2</sup>

(6 ml/kg) with adequate PEEP level (at least 3–5 cmH<sup>2</sup>

ther delay (within the first 5–7 days of mechanical ventilation).

feeding is achieved once there is no more gastrointestinal paresis.

**Table 6.** Pulmonary artery hypertension monitoring and right ventricular dysfunction prevention.

In case of concomitant LV insufficiency and signs of systemic hypoperfusion (with raising of LAP/PCWP and sudden reduction of CO, CI, and SvO2 ), we will need to increase the inotrope support and try to compensate the peripheral vasoconstriction with peripheral vasodilators as nitroprusside, when the MAPs allow to do that, in order to reduce left ventricle afterload and facilitate the ejection. The conditioning with inodilators as levosimendan [10] can be very helpful and, in case of massive peripheral vasodilatory response, it can be compensated with mean dosage of noradrenaline to ensure adequate MAPs. When this is not enough, an additional support with IABP should be considered, but, when insufficient, a central or peripheral VA-ECMO will be placed. The simultaneous presence of the IABP will help avoid pulmonary edema by reducing the afterload of LV.

#### **7.5. Avoid metabolic acidosis and monitor acid-base balance and kidney function**

A patient undergoing heart transplant comes from a long period of low cardiac output, so the kidney dysfunction is often preexisting.

In the immediate postoperative period, urinary output may decrease for several reasons including intravascular volume depletion and kidney damage coming from long lasting extracorporeal support or from the use of unbalanced solutions for fluid challenge. In addition, a high use of colloidal molecules may damage directly the renal tubules with a process called "osmotic-nephrosis." If urine output is <0.5 ml/kg/h despite optimization of blood pressure, preload and CO, and use of standard diuretics (furosemide or torasemide), and the patient develops kidney failure with serum urea >200 mg/dL or hyperkalemia, kidney replacement therapy becomes mandatory.

We prefer early application of continuous venovenous hemofiltration (CVVH) for a complete hemodynamic and fluid rebalancing. In case kidney replacement therapy is necessary in a long-term postoperative period, the change is made to intermittent dialysis (three times weekly).
