Добавил:

Sekretar kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.

Вуз:

Ростовский Государственный Медицинский Университет

Предмет:

Медицина общая

Файл:

Книга_3901_Библиотеки_им_академика_М_И_Перельмана

.pdf

Скачиваний:

Добавлен:

10.10.2026

Размер:

9 Мб

Скачать

☆

<<< < Предыдущая 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 2122 / 2322 23 > Следующая >>>

of air in the arterial circuit, can result in occlusion of

major arteries and arterioles, resulting in end-organ

ischemia. Air in the coronary arteries presents as

acute ST-elevation ischemia and may result in pro-

found myocardial dysfunction and inability to separ-

ate from CPB, while cerebral arterial gas embolism

may result in stroke, seizure, or impaired neurocog-

nitive function postoperatively. Any microbubbles

can transfer directly into the patient’s microcircula-

tion with the potential to cause harm through diffuse

impairment of gas exchange in the capillary bed. Air

in the venous lines can cause an air lock, preventing

venous drainage and necessitating a rapid reduction

of forward flow in order to prevent emptying of the

venous reservoir.

Air embolism during cardiac surgery is a compli-

cation with potentially severe or fatal consequences.

Even if recognized and treated immediately, it can

cause significant and irreversible neurological injury.

A sudden and rapid drop in the cerebral oximetry

readings without an obvious alternative explanation

should give rise to a high index of suspicion for

cerebral arterial gas embolism. Transesophageal echo-

cardiography can potentially help in identifying air in

the aorta.

The primary goal for managing this complication

is protecting the brain. Measures include:



Identifying the location of air entry and

preventing further air from entering

the circulation.



Supine positioning. Steep Trendelenburg

positioning had previously been thought to help

expel air bubbles from the cerebral circulation,

however, this is now not recommended, as placing

the patient head-down can exacerbate

cerebral edema.



Decreasing cerebral oxygen demand, which can be

achieved pharmacologically with medications

such as propofol, as well as by actively cooling the

patient. Cerebral oxygen demand decreases by

approximately 7% for each degree Celsius that the

patient is cooled (see also Chapter 18). Active

cooling is easily achieved on CPB once the source

of air has been identified and eliminated and flow

has been reestablished. Emergent initiation of

deep hypothermia has also been successfully

supplemented with retrograde cerebral perfusion

in several cases, whereby oxygenated blood is run

retrograde via superior vena cava cannulation

with resultant purge of arterial gas into the

arch effluent.



Treatment with IV methylprednisolone has been

considered with the goal of minimizing the

inflammatory damage secondary to ischemia and

subsequent reperfusion, although the efficacy is

not clear.



Intravenous lidocaine may be beneficial.



Definitive treatment for cerebral arterial gas

embolism includes hyperbaric oxygen therapy.

In addition to decreasing oxygen demand, the other

goal in this situation is to maintain adequate oxygen

delivery to tissues, which can be achieved with nor-

movolemia and adequate perfusion pressure.

Hemodilution to a hematocrit of ~30% may be bene-

ficial. The most common causes leading to air in the

CPB circuit are summarized in Table 20.4.

Electrical Failure

All hospitals should have multiple levels of power

supplies, with backup generators that switch in with-

out delay when mains power fails. While the inci-

dence of multi-level power fa ilures is rare, they do

occur, and strategic planning needs to be included in

local protocols.

Most contemporary HLMs have a battery backup

built into the system. These need to be maintained to

assure best battery performance. Keeping a hand

crank on each HLM is mandatory in case of total

electrical failure. Although practices such as making

sure the HLM’s battery is fully charged, that the

machine is plugged into a wall socket that is fed by

the hospital backup system and that the hand crank is

present seem totally intuitive, it is advised to include

them in the pre-CPB checklist to assure high

reliability.

On occasions where a single pump dies, a spare

pump module should be available for immediate use.

Clinicians need to make sure during setup that the

tubing is long enough to be moved to a different

module. Failure of the electronic control panel or

the recording system are mostly software issues and

can often be dealt with by rebooting the system.

Modern HLMs should be able to be run with just

manual control, independent of the electronic system.

Heater Cooler Failure

The heating/cooling device is a major component of

cardiopulmonary bypass. A backup device or an

Gregory M Janelle, Jane Ottens and Michael Franklin

200

alternative method to rewarm a patient should be

available. These devices must be maintained in

accordance with their IFU to minimize mycobac terial

growth. Meticulous maintenance is particularly

important, highlighted by the impact of mycobacter-

ium chimaera, as continual disinfection may cause

faults due to the corrosive nature of chemicals used.

A backup heater/cooler or similar device from an

ECMO circuit should be available at all times. If this is

not the case a roller pump with a loop of tubing

attached to 2 Hansen connectors, sitting in a bucket

of warm water can allow some temperature control

until a more permanent solution has been found.

Clinical Events

Numerous clinical events may result in CPB disasters.

The following are summaries of some of the more

prevalent clinical events that have been previously

reported in the Australian and the UK perfusion

incident reporting systems.

Drug and Medication Error

This topic represents the second highest number of

incidents reported to PIRS-2 (Figure 20.4). Teamwork

and excellent communication, preferably in the form

of closed loop communication, are important so each

member of the team is aware of allergies, religious

beliefs (e.g. Jehovah’s Witness) and when drugs are

given (especially heparin and protamine). Table 20.5

compiles a select few of the more common drug

errors and ways to prevent them.

Table 20.4. Causes of air entrainment into CPB circuit

Vent tubing backwards

Purge lines open

Failure/inactivation of low-level alarm or bubble

detectors; venous line occlusion with subsequent

draining of reservoir

Membrane fiber leak

Vacuum drainage with excessive negative pressure

Inattention/distraction of perfusionist

Countermeasures

Vent tubing



Pre-bypass checklist



Check suckers with

blood/saline before

commencing CPB



One-way valve in

all vents

Level alarm, bubble

detectors

Tested, connected and

servo regulated

Positive and negative

pressure valves intact

Positive and negative

pressure is measured

and alarmed when

vacuum is used

Decrease venous embolic

load



Snare venous

cannula to prevent

(further) air from

entering



Partially clamp

venous line

Table 20.5. Common drug errors

Incorrect drug labeling

Out of date drugs used

Heparin not given or given in wrong dose or at

inappropriate time

Protamine given while pump suckers activated

Cardioplegia solution with too much/too little

potassium

Cardioplegia delivered systemically before cross-

clamping of aorta

Incompatible blood group transfusion

Anesthetic gas vaporizer on HLM left open after CPB

Countermeasures

Double-check drugs including reading label and dates on

vials and syringes, use of appropriate labelingsystem

Commence CPB only after all team members have

confirmed safe ACT

Suckers are turned off and removed from chest when

anesthesiologist announces that protamine is about

to start

Confirm blood/cardioplegia ratio before operation; check

potassium concentration with blood gas analysis

Use end-of-CPB checklist to ensure HLM is stripped

down correctly

Chapter 20: Common and Uncommon Disasters during Cardiopulmonary Bypass

201

Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/

Heparin Resistance

Heparin is the most common anticoagulant used for

cardiopulmonary bypass. The standard heparin dose

is 300–500 IU/kg, the target ACT varies between

institutions but generally is somewhere between

400 and 550 seconds. Failure to achieve the ACT goal

despite repeated heparin doses up to 600 IU/kg is

defined as heparin resistance. In the event of an inad-

equate response to heparin, it is a Class 1A recom-

mendation of the Society of Thoracic Surgeons and

Society of Cardiovascular Anesthesiologists that

recombinant antithrombin III be used to improve

heparin sensitivity. If not treated adequately, heparin

resistance could result in subtherapeutic anticoagula-

tion, potentially leading to oxygenator failure, throm-

boembolic phenomena and patient death. Alternative

anticoagulants such as bivalirudin or argatroban

should be considered in cases where heparin resist-

ance is not due to inadequate antithrombin III levels

(see also Chapter 6 for more detail).

Cold Agglutination

Cold agglutinins are IgM antibodies directed against

red blood cells. They are inert at physiological body

temperatures and have a variable temperature thresh-

old below which they become active (thermal ampli-

tude). Depending on this threshold they might

become activated during hypothermic bypass. Once

activated they agglutinate erythrocytes, which in turn

fix to activated complement, leading to irreversible

cell damage. Severe hemolysis occurs when the blood

temperature is (i) cold enough for the antibody to be

active and (ii) warm enough for complement to be

active. Surgeons wearing magnifying loops or perfu-

sionists observing their cold cardioplegia circuit are

often the first ones to spot any agglutination.

Normothermia, avoiding cold cardioplegia and flush-

ing the coronaries with warm cardioplegia before

removing the aortic cross clamp are the mainstays

of managing patients with known cold agglutinins

or sudden onset of hemolysis (see Chapter 16 for

more detail).

Malignant Hyperthermia

Malignant hyperthermia (MH) is the result of a reac-

tion to specific triggering agents in patients with

myopathies typically affecting the type 1 ryanodine

receptor. This condition is hereditary and transmitted

in an autosomal dominant pattern. There often is a

family history of malignant hyperthermia that will be

reported in preoperative assessment. When a malig-

nant hyperthermia crisis is triggered, a hypermeta-

bolic state is induced in which there is a massive

and unchecked release of calcium from the sarcoplas-

mic reticulum of skeletal muscle. This triggers a cas-

cade of derangements, including hyperthermia,

tachycardia, hyperkalemia, hypercapnia, muscular

breakdown and metabolic acidosis. It is often noticed

first by the surgeon, noticing unusual chest wall rigid-

ity or that the patient feels warm. Blood gases confirm

that CO

rises fast despite increasing sweep gas flow.

Metabolic acidosis, excessive temperature despite

cooling and hematuria are also typical warning signs.

In cases of preoperatively known or suspected

malignant hyperthermia the anesthesiologist and per-

fusionist should discuss the anesthetic plan, including

avoidance of all triggering agents such as succinylcho-

line and volatile anesthetic agents, as well as flushing

the anesthesia machine with O

and removing the

vaporizer from HLM.

In the event of a MH crisis all potential triggering

agents have to be stopped immediately and removed

from continuity with the patient. The ventilator cir-

cuit and CO

absorber canister should be replaced

with new components, the patient has to be treated

with dantrolene and the surgical procedure should be

terminated as soon as reasonably possible. The

Malignant Hyperthermia Association of the United

States maintains a 24-hour hotline and additional

resources to help prepare for and provide real time

assistance to acutely manage a malignant hyperther-

mia crisis. Similar helplines are available in most

countries around the world.

Vasoplegic Shock

Systemic vasodilation, often refractory to standard

therapies, is a dangerous complication of cardiopul-

monary bypass. It is thought to be associated with a

systemic inflammatory response that can be precipi-

tated by the patient’s circulation interacting with the

foreign materials of the bypass circuit. It may also

result from a reaction of common anesthetics with

certain drug classes, including but not limited to

angiotensin converting enzyme inhibitors and angio-

tensin II receptor blockers. The vasoplegic patient is

unable to achieve adequate end-organ perfusion due

to hypote nsion in spite of adequate or supra-normal

cardiac output. In some cases, this can make it impos-

sible to safely separate from CPB if not adequately

treated. Treatment options include vasopressors, such

as norepinephrine, vasopressin, intravenous

Gregory M Janelle, Jane Ottens and Michael Franklin

202

methylene blue and vitamin B12 (hydroxycobalamin),

as well as newer agents such as angiotensin II.

Aortic Dissection

Manipulation or instrumentation of the aorta can

cause disruption of the intima and acute dissection

of the vessel. This occasionally occurs during aortic

cannulation or at proximal coronary graft anasto-

mosis sites. It is critical to identify this complication

early. As a consequence of cannulating a dissected

aorta, there may be loss of radial arterial line wave-

form or elevated line pressure when attempting to go

on bypass and the aorta may begin to appear dilated

and discolored. Intraoperative transesophageal echo-

cardiography, as well as epiaortic ultrasound, can be

used to identify or confirm this diagnosis.

This complication needs to be treated immedi-

ately. Depending on the extent of the damage done

this can require surgery ranging from an ascending

aortic interposition graft to a complete aortic arch

replacement.

Over-pressurization during Cardioplegia

Over-pressurization during anterograde or retrograde

cardioplegia can occur. Monitoring the pressure in

the delivery system and taking the pressure drop in

the aortic root or the coronary sinus into account can

avoid cardiac injury. Consequences of over-

pressurization of the retrograde system include cor-

onary sinus rupture, and more commonly, epicardial

petechiae and myocardial edema from extravasation

of high pressure cardioplegia. Over-pressurization of

the aortic root during antegrade cardioplegia can

result in direct injury to the aortic root or valve. The

root is typically monitored visually by the surgeon

and a Y-connector can be used to vent the root when

needed. Anterograde cardioplegia catheters with inte-

grated overpressure relief valves are commercially

available.

Inadvertent Cannulation of Hepatic Vein during

Bi-caval Venous Cannulation

Advancing the inferior vena cava cannula too far

during bi-caval cannulation is not uncommon.

Inadvertent placement into the hepatic vein can lead

to poor venous drainage, hepatic venous congestion

with potential hepatic dysfunction and efferent

venous obstruction of visceral organs and the kidneys.

Transesophageal echocardiography can be used to

confirm proper cannula placement and assist with

repositioning.

This chapter highlights commonly reported incidents

in current perfusion practice. New forms of compli-

cations arise as our HLMs become more complex and

feature integration with monitoring and electronic

medical records. In order to run a highly reliable

perfusion service it is essential that protocols and

procedures for dealing with accidents and unforeseen

events are regularly updated to include new equip-

ment or technology as it is added to our arsenal of

tools.

Suggested Further Reading

1. Reason J. Human error: models

and management. BMJ. 2000; 320

(7237):768–770.

2. Wilcox TW, Baker RA. Incident

reporting in perfusion: current

perceptions on PIRS-2.

J Extracorp Tech 2020; 52:7–12.

3. Darling E, Searles B. Oxygenator

change-out times: the value of a

written protocol and practice

simulation exercises. Perfusion

2010 May; 25(3):141–143;

discussion 144–145.

4. Uysal S, Lin HM, Trinh M et al.

Optimizing cerebral oxygenation

in cardiac surgery: a randomized

controlled trial examining

neurocognitive and perioperative

outcomes. J Thorac Cardiovasc

Surg 2020; 159(3):943–953.e3

5. Ferraris VA, Brown JR, Despotis

GJ et al. Special report: STS

workforce on evidence based

surgery. 2011 update to the

Society of Thoracic Surgeons and

the Society of Cardiovascular

Anesthesiologists blood

conservation clinical practice

guidelines * The Society of

Thoracic Surgeons Blood

Conservat. ATS. 2011;91

(3):944–982.

6. Shore-lesserson L, Baker RA et al.

The Society of Thoracic Surgeons,

The Society of Cardiovascular

Anesthesiologists and The

American Society of

ExtraCorporeal Technology:

Clinical practice guidelines –

anticoagulation during

cardiopulmonary bypass. Ann

Thorac Surg. 2018;105

(2):650–662.

7. Gulabani M, Gurha P, Ahmad S

et al. Intra-operative post-

induction hyperthermia, possibly

malignant hyperthermia:

anesthetic implications, challenges

and management. J Anaesthesiol

Clin Pharmacol. 2014;30

(4):555–557.

Chapter 20: Common and Uncommon Disasters during Cardiopulmonary Bypass

203

Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/

8. Still RJ, Hilgenberg AD, Akins

CW et al. Intraoperative aortic

dissection. Ann Thorac Surg.

1992;53(3):374–379.

9. Assaad S, Geirsson A, Rousou L

et al. The dual modality use of

epiaortic ultrasound and

transesophageal echocardiography

in the diagnosis of intraoperative

iatrogenic type-a aortic dissection.

J Cardiothorac Vasc Anesth. 2013

Apr;27(2):326–328.

Gregory M Janelle, Jane Ottens and Michael Franklin

204

Index

abciximab, 157–158

abdominal tumors, 126

acetate, 46

acid-base management, 85, 94,

115–116

activated clotting time (ACT), 30–31,

50–52

acute aortic syndrome, 58

acute kidney injury (AKI), 184

CKD management, 192

definitions and scores, 184–185

epidemiology and outcomes,

184–185

extracorporeal life support, 136

pathophysiology, 185–186

prevention, 190–192

risk factors, 186–188

acute normovolemic hemodilution

(ANH), 83–84, 162

acute respiratory distress syndrome

(ARDS), 123, 170–171

adrenaline, 119

after-drop, 63–64, 85

afterload, during weaning from CPB,

118

air bubble detectors, 28–29, 35–36

air embolism

during aortic root cannulation,

59–60

with centrifugal pumps, 18

in circuit, 199–201

de-airing for prevention, 112–113

filters and bubble traps, 20

–22

priming, 42

with reservoir emptying, 18

with venous cannulation, 61–62

air lock, 14, 61–62

Air Protection System (APS), 40

alarms, heart-lung machine, 28–29, 115

albumin priming solution, 45

Allen formula, 43–44

alpha agonists, 93–94

altered heparin resistance, 53

Andexanet-α, 158

anemia, 161–164

anesthesia

gas scavenging system, 35

myocardial protection, 111

neuroprotection, 86, 179, 181

weaning from CPB, 115

angiotensin converting enzyme

inhibitors (ACE-I), 172, 190

angiotensin receptor blockers, 190

antegrade cardioplegia, 108–109

antegrade cerebral perfusion (ACP),

87–88

anterior mediastinal mass, 125–126

anti-arrhythmic drugs, 113–114, 117

anticoagulation, 49. See also heparin

direct thrombin inhibitors, 54–55

future, 55–56

MiECC, 73

monitoring, 30–31

, 50–52

novel oral anticoagulants, 158

pediatric patients, 152

reinstitution of CPB, 119

reversal, 53–54, 118

vitamin K antagonists, 157–158

anti-diuretic hormone (ADH), 121

antifibrinolytic agents, 85–86, 161–162

anti-inflammatory interventions

perfusion strategies, 172–173

pharmacological strategies, 172

antiplatelet agents, 157–158

anti–Xa activity, 51–52

aortic aneurysm, 81–82, 126–129

aortic cannulation, 12–13

aortic cross-clamping, 110, 183

aortic dissection, 203

aortic root cannulation, 58–60,

108–109

apixaban, 158

aprotinin, 85–86, 161–162

argatroban, 54–55

argipressin, 121

arrhythmia, during weaning from CPB,

113–114, 117

arterial blood path obstruction, 197

arterial cannula, 12–14

designs, 12–13

flow profiles, 13

performance index, 57–58

arterial cannulation, 57–58

complications, 59–60

connection, 58–59

DHCA, 81, 83

pediatric patients, 152

peripheral, 60

arterial line filters, 21–22, 35–36

arteriovenous (AV) loop, 35–36

aspartate, 107

aspirin, 157–158

AT3 deficiency, 53

atherosclerosis, 58–59, 175, 178, 180,

183

autologous blood priming, 42–44, 154

autoregulation

cerebral, 86, 177

kidney, 187–190

axillary arterial cannulation, 13–14, 60

barbiturates, 86, 181

battery backup unit, 35

benzodiazepines, 99

bicaval cannulation, 14–15, 61–62, 152

203

biocompatible tubing, 11–12, 172

bivalirudin, 54–55

bleeding

assessment, 158–161

causes, 156–158

gastrointestinal, 169

management, 159–161

blood, 162

cold agglutinins, 164, 202

Jehovah’s Witnesses, 162–163

sickle cell anemia, 163–164

blood cardioplegia, 105–107

blood conservation, 85–86, 156,

161–162

antifibrinolytic agents, 85–86,

161–162

cardiotomy suction, 66–68, 162

cell salvage, 21, 68, 71, 97–98, 118,

162

MiECC, 73–74

blood flow. See also flow rates

cerebral, 86, 175, 177

hemodilution, 42–

kidney, 187–190

monitoring, 25–26

obstruction, 197

parameters for adequate perfusion,

92–93

splanchnic, 168–170

blood gas analysis, 29–30, 94–95, 100,

180, 195–197

205

Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/

blood gas management

alpha stat management, 85, 100

during DHCA, 85

parameters for adequate perfusion,

93–94

for pediatric patients, 153

pH-stat, 20, 100, 153

temperature effects on, 100

blood pressure, 175

AKI risk, 186–187

cerebral blood flow, 177

delirium, 177

stroke, 176–177

blood priming, 42–44, 154

bowel ischemia, 169

Bretschneider’s solution, 105–107

briefing, preoperative, 7

bubble detectors, 28–29, 35–36

bubble traps, 20–22

calcium, 46, 97, 115, 121, 151

calcium channel blockers, 181

calibration, monitoring systems, 29

cannulation. See also arterial

cannulation; venous

cannulation

aortic, 12–13

aortic root, 58–60, 108–109

axillary arterial, 13–14,

bicaval, 14–15, 61–62, 152, 203

cavo-atrial, 14–15, 61–62

coronary sinus, 65–67, 109

femoral, 13–14, 60, 62

inferior vena cava, 62

peripheral arterial, 60

peripheral venous, 62–63

right atrial, 61–62, 65–67

subclavian, 13–14

superior vena cava, 62

carbon dioxide (CO

) flushing, 36

carbon dioxide production (VCO

), 30,

95–96

cardiac arrest. See also cardioplegia

accidental hypothermic cardiac

arrest, 134–135

cardiogenic shock, 135–136, 138

cardioplegia, 103–104, 111

delivery, 22–23, 107–108

antegrade, 108–109

minimal access surgery, 109–110

preparation and setup, 35

retrograde, 109

through vein grafts, 109

history, 102–103

in MiECC, 73–74, 109–110

monitoring, 27–28

over-pressurization during, 203

pediatric patients, 151

physiology, 103–105

temperature, 110

cardiopulmonary bypass (CPB). See

also weaning from CPB; specific

topics

conduct, 57

connection of patient to circuit,

62–63

initiation, 63

monitoring, 64–68

pediatric patients, 152–153

pressure management, 64–68

rewarming,

63–64

temperature management, 63–65

venous cannulation, 61–63

history, 9–10, 123

MiECC practical lessons, 77–78

registries, 33

cardiopulmonary bypass (CPB) circuit

air in, 199–201

carbon dioxide flushing, 36

components, 11, 34

filters and bubble traps, 20–24,

172

hemofilters, 23–24, 154, 162, 172

suckers and vents, 22, 36, 68–69

tubing, 9–12, 35–36, 172

typical configuration, 9–10

disruption, 198–199

failure, 197–198

MCS, 123–125

priming, 36–37

hemodilution with, 42–44, 162

solutions, 42–47

setup, 34–36, 40

DHCA modifications, 82–83

human factors, 37

minimally invasive extracorporeal

circulation, 40

pre-bypass checklist, 37–40

pre-bypass patient concerns, 38,

cardiopulmonary bypass (CPB)

machine. See heart-lung

machine

cardiotomy suction, 66–68, 162

cavitation, 61–62

cavo-atrial cannulation, 14–15, 61–62

cell salvage, 21, 68, 71, 73–74, 97–98,

118, 162

central venous pressure (CVP), 65

centrifugal pump, 16–18, 73–74,

123–125

CentriMag, 147

cerebral blood flow (CBF), 86, 175, 177

cerebral cooling, 84

cerebral embolism, 112–113, 175, 178,

180, 183

cerebral ischemia, 175, 183

blood pressure control, 176–177

monitoring, 30, 177–180

pharmacological cerebral protection,

178–182

risk factors, 175–176

temperature management, 182–183

cerebral metabolic rate (CMRO

), 86,

cerebral oxygen saturation

CPB changes, 166–167

during DHCA, 84, 88

monitoring of, 30, 177–180

neurological complications, 177–180

cerebral perfusion strategies

intermittent cerebral perfusion,

86–87

for pediatric patients, 151–152

retrograde cerebral perfusion, 59–60,

87–88

selective antegrade cerebral

perfusion, 87–88

cerebrospinal fluid (CSF) drainage, 89

checklist, 37–38

chloride, imbalances, 97–98

chronic kidney disease (CKD),

186–187, 192

chronic thromboembolic pulmonary

hypertension (CTEPH), 90

circuit pressures, 27–28

citrate-phosphate-dextrose (CPD), 107

clopidogrel, 157–158

clot formation, 49

clotting factors, 43, 49–50

coagulopathy

assessment, 158–161

blood conservation techniques,

85–86, 156, 161–162

pathophysiology, 156

preoperative medication, 156

–157

antiplatelet agents, 157–158

novel oral anticoagulants, 158

vitamin K antagonists, 157–158

therapeutic interventions and

management, 159–161

cold agglutinins, 164, 202

colloid priming solutions, 45

communication

solutions to improve, 5

preoperative briefing and

postoperative debriefing, 7

standardized conversations, 5

during weaning from CPB, 112

congenital heart disease, 150. See also

pediatric patients

cooling, 84

coronary air embolism, 112–113

coronary artery bypass graft (CABG),

110, 173, 190

coronary sinus cannulation, 65–67, 109

corticosteroids, 47, 172, 181

Index

206

cryoprecipitate, 159–161

crystalloid cardioplegia solutions,

105–107

crystalloid priming solutions, 43–45

culture of safety, 194–195, 198–199

custodiol solution, 105–107

cyclosporine, 111

dabigatran, 158

de-airing, heart, 112–113

deep hypothermic circulatory arrest

(DHCA), 80, 90, 99

indications, 80–81

monitoring during, 80–81, 85, 88–90

neuroprotection during, 86

hypothermia alone, 86–88

intermittent cerebral perfusion,

86–87

pharmacological, 86, 181

retrograde cerebral perfusion,

87–88

selective antegrade cerebral

perfusion, 87–88

spinal cord, 88–90

pediatric patients, 151–152

perfusion considerations

acid-base management, 85

blood conservation, 85–86

circulatory arrest, 84–85

cooling, 84

extracorporeal circulation, 82–83

glucose management, 85

hemodilution, 83–84

rewarming, 85

temperature management, 84–85

physiological effects, 80, 82

preoperative considerations, 80–81

pulmonary (thrombo)

endarterectomy, 86–87, 90

safe duration, 86

spinal cord protection during, 88–90

surgical considerations, 81–83

Del Nido Cardioplegia (DNC),

106–107

delirium, postoperative, 177

1-desamino-8-D-arginine-vasopressin

(DDAVP), 161

descending thoracic aortic aneurysm

(DTAA), 81–82, 126–129

dexmedetomidine, 191–192

diastolic augmentation, 138, 141

difficult airway, 125–126

direct acting oral anticoagulants

(DOACs), 158

direct current cardioversion (DCCV),

117

direct ostial cardioplegia, 109

direct procurement and perfusion

(DPP), 129, 131

direct thrombin inhibitors (DTIs),

54–55

disasters during CPB, 194–195, 203

air in circuit, 199–201

blood path obstruction, 197

circuit disruption, 198–199

electrical failure, 200

equipment failure, 197–198

falling cerebral oxygen saturation,

197–198

heater cooler failure, 200–201

incident reporting and safety culture

in prevention, 194–195,

198–199

oxygenator failures, 195–197

dobutamine, 119

donation after brain stem death (DBD),

129

donation after cardiac death (DCD),

129–131

donor organs

heart, 129–131

lung, 129–132

dopamine, 119

drug bioavailability, 43

drug error, 201

drug metabolism, 98–99

echocardiography. See transesophageal

echocardiography

elastometry, 158–159

electrical failure, 200

electrocardiogram (ECG), 31, 65

electroencephalography (EEG), 84

electrolyte management, 45–47, 96–98,

115–116

electronic perfusion data, 31–33

embolism. See also air embolism

aortic root cannulation and

atherosclerotic, 58–59

cerebral, 112–113, 175, 178,

180, 183

detection, 178, 180

pulmonary, 90

endothelial activation, 167–168

endotoxins, 168–169

enoximone, 119–121

epiaortic ultrasound (EAU), 58–59, 183

epicardial pacing, 114

epinephrine, 119

epsilon-aminocaproic acid (EACA),

161–162

eptifibatide, 157–158

error, 37. See also disasters during CPB

human factors perspective on, 2–3,

Safety 1 and Safety 2 perspectives on,

1–2

esmolol, 107

evoked potential monitoring, 89–90

ex vivo lung perfusion (EVLP),

129–132

extracellular cardioplegia solutions,

105–107

extracorporeal cardiopulmonary

resuscitation (ECPR), 134

extracorporeal circuit. See

cardiopulmonary bypass circuit

extracorporeal life support (ECLS), 71

accidental hypothermic cardiac

arrest, 134–135

trauma patients, 135–136

extracorporeal membrane oxygenation

(ECMO). See also veno-arterial

extracorporeal membrane

oxygenation

backup during equipment failure,

197–198

centrifugal pumps in, 18

failure to wean from CPB, 122

history, 9

–10, 123

MCS with, 123–125, 140

emergent or bail-out applications,

133–136

lung transplantation, 132–133

thoracic surgeries using, 125–126

factor concentrates, 157–158, 161

factor II inhibitors, 158

factor Xa inhibitors, 158

femoral cannulation, 13–14, 60, 62

fenoldopam, 191–192

fibrillation induction, 110

fibrinogen concentrate, 161

fibrinolysis, 156, 161–162

filters, 20–24, 172

filtration, 23–24, 36–37, 154, 162, 172

flow rates

acid-base management, 116

AKI risk, 186–187

heart-lung machine monitoring of,

25–26

oxygen delivery, 166–167

pediatric patients, 152

targets for adequate perfusion, 92–93

fluid overload, 191–192

flushing, CPB circuit, 36

fresh frozen plasma (FFP), 157–161

gas exchange

monitoring, 29

cerebral oxygen saturation, 30,

177–180

in-line blood gas analysis, venous

saturation and hematocrit

monitors, 29–30, 94

oxygen delivery and carbon

dioxide extraction, 30

oxygenator, 19–20

Index

207

Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/

gas scavenging system, 35

gas supply system, 20

gaseous microemboli (GME), 61–62

gastrointestinal (GI) dysfunction,

168–170

GDP ratio, 96

Gelofusine priming solution, 45

glucose

management, 85, 98, 116, 191–192

priming solution, 46–47

glutamate, 107

glyceryl trinitrate (GTN), 121

glycoprotein IIb/IIIa inhibitors,

157–158

goal-directed perfusion (GDP), 95–96

gravity siphoning, 61

Gritten Report, 34, 37

Haemaccel priming solution, 45

Harlequin Syndrome, 143

heart, damage during CPB, 171. See

also myocardial protection

heart failure, stratification of, 144–145

heart-lung machine (HLM), 194

alarms, 28–29, 115

components, 11, 34

development, 9–10

failure, 197–198

gas supply system, 20

MCS with, 123–125

monitoring, 25–29

oxygenators, 19–20, 35, 195

–197

preparation and setup, 34–36, 40

human factors, 37

minimally invasive extracorporeal

circulation, 40

pre-bypass checklist, 37–40

pre-bypass patient concerns, 38,

priming, 36–37

hemodilution with, 42–44, 162

solutions, 42–47

pump heads, 14–18

reservoirs, 18–19

heart rate, during weaning from CPB,

113–114

heart transplantation, 129–132

heart venting, 68–69

heart-lung transplantation, 132

HeartMate 3, 147

HeartWare HVAD, 147

heat exchanger, 19–20, 22, 34–35

heater cooler failure, 200–201

hematocrit (Hct)

AKI risk, 186–187

deep DHCA, 83–84

factors affecting, 43–44

monitoring, 29–30, 94

optimal values, 42–43

parameters for adequate perfusion,

93–

hemodilution, 42

AKI risk, 186–187

avoidance, 156, 162

blood flow, 42–43

clotting factors, 43

control, 43–44

during DHCA, 83–84

drug bioavailability, 43

drug metabolism effects, 98–99

in pediatric patients, 153–154

hemodynamic monitoring, 31, 73, 76,

178, 180

hemofilters, 23–24, 154, 162, 172

hemoglobin, during weaning from

CPB, 116

hemolysis, 18, 28, 66–67, 92–93,

185–187, 202

heparin, 49, 54–56

dosing, 49–51

monitoring, 30–31, 50–52

neutralization, 53–54, 118

for pediatric patients, 152

pharmacology, 49–50

in priming solution, 47

rebound, 54, 156

resistance to, 53, 202

thrombocytopenia induced, 54–55

tubing containing, 11–12, 172

heparin-induced thrombocytopenia

(HIT), 54–55

hepatic dysfunction, 169–170

hepatic vein, inadvertent cannulation

of, 203

histidine-tryptophan-ketoglutarate

(HTK), 105–107

homeostasis, 92, 166–167. See also

metabolic management

human factors, 1–3, 37, 194, 198

hydroxyethyl starch (HES), 45,

191–192

hyperchloremia, 97–98

hyperglycemia, 46–47, 85, 98, 116,

191–192

hyperkalemia, 46, 96–97, 115

hyperlactatemia, 95

hyperoxia, 150–151

hypertension, 175

hyperthermia, 85, 100–101, 182–183

hypocalcemia, 46, 97

hypoglycemia, 116

hypokalemia, 46, 96–97, 115

hypomagnesemia, 46, 97

hyponatremia, 45–46

hypophosphatemia, 97

hypotension, 175, 177

hypothermia. See also deep

hypothermic circulatory arrest;

hypothermic cardiac arrest;

rewarming

adverse effects, 100

AKI risk, 186–187

bleeding management with, 159

blood gas management, 85, 100

coagulopathy associated with, 156

drug metabolism effects, 98–99

metabolic management, 99–101

monitoring, 26–27, 65, 80–81, 85

myocardial protection, 102, 110–111

neuroprotection, 86–88

physiological effects, 80, 82

sickle cell anemia, 163–164

venous saturation, 94–

hypothermic cardiac arrest (HCA),

134–135

idarucizumab, 158

Impella, 138–139, 146

incident reports, 194–195, 198–199

inferior vena cava (IVC), 62, 126

inflammation. See systemic

inflammatory response

inhalational anesthetic agents. See

volatile anesthetic agents

in-line blood gas analysis, 29–30, 94

inotropic support, 115, 117–121

insulin, 46–47, 98, 116

insulin resistance, 85

Interagency Registry of Mechanically

Assisted Circulatory Support

(INTERMACS), 144–145

intercostal artery perfusion, 127–129

intermittent cerebral perfusion, 86–87

intermittent cross-clamping/fibrillation

(ICC), 110

international normalized ratio (INR),

157–158

intra-aortic balloon pump (IABP),

65–66, 68, 117

failure to wean from CPB, 122

MCS with, 138–140

complications, 140

indications, 140

management of patients with, 139

physiological effects, 141

intracellular cardioplegia solutions,

105–107

intrathecal pressure (ITP),

ischemia. See also cerebral ischemia

gastrointestinal, 168–169

myocardial, 102–103, 151

pancreatic, 170

ischemia-reperfusion injury

coagulopathy, 156

cold reperfusion for prevention, 85

lung, 173

myocardial, 102–103

Index

208

in pediatric patients, 150–151

ischemic preconditioning, 102,

110–111, 190

Jehovah’s Witnesses, 162–163

jugular venous oxygen saturation, 88

ketamine, 179–181

kidney, blood flow and oxygen delivery

to, 187–190

kidney injury. See acute kidney injury

kinetic-assisted venous drainage

(KAVD), 28, 73–74

lactate, 46, 93, 95, 116

latent failures, 1–2

latex rubber tubing, 11

leaks, CPB circuit, 198–199

left atrial (LA) pressure, 65

left heart bypass (LHB), 81–82,

126–127

left ventricle (LV) distension, 65–66,

68–69

left ventricular assist device (LVAD),

146–148

leukocyte depletion, 172–173

levosimendan, 121

lidocaine, 181

liver dysfunction, 169–170

liver transplantation, 133

low level alarm, 28–29

low-molecular-weight heparin

(LMWH), 54

lung.