CHANGEMENTS PHYSIOLOGIQUES

LORS DES CHIRURGIES

AORTIQUES

André Grenier md

Anesthésiologiste

TABLE I

Elective abdominal aortic aneurysm resection

mortality rates (%)

The range of reported mortality rates for elective abdominal aortic

aneurysm resection. (Composite figures from data reported in

references 4-15).

1960-1969

1970-1915

1976-1986

9-18

4-9

1-6

TABLE II

Abdominal aortic surgery - coexisting disease

states

Heart disease

Previous myocardial infarct 40-50

Angina 10-20

Congestive heart failure 10-15

Hypertension 50-60

Chronic obstructive pulmonary disease 25-50

Diabetes Mellitus 9-12

Renal impairment 5-17

The range of coexisting disease states (%) reported in association with

abdominal aortic surgery. (Composite figures from data reported in references

9-10, 15, 30-41.)

None

Clinical CAD

Normal coronary arteries

Mild to moderate CAD

Advanced compensated CAD

Severe, correctable CAD

Severe, inoperable CAD

14

49

22

14

1

21

99

192

188

54

4

18

34

34

10

CAD, coronary artery disease

Data from Hertzer NR, Beven EG, Young JR, et al: Coronary artery disease in peripheral

vascular patients. A classification of 1000 coronary angiograms and results of surgical

management. Ann Surg 199:223-233, 1984.

RESULTS OF CORONARY ANGIOGRAPHY IN 1000

PATIENTS WITH PERIPHERAL VASCULAR DISEASE

Suspected Total

64

218

97

63

4

85

317

289

251

58

8.5

32

29

25

5.8

Angiographic Classification No. % No. % No. %

SERVICE DE CHIRURGIE VASCULAIRE

CENTRE HOSPITALIER UNIVERSITAIRE DE QUÉBEC

CENTRE DE SANTÉ

VASCULAIRE

CHIRURGIE ÉLECTIVE AAAN Moyenne annuelle

1986-1990 245 49

1991-1995 368 73.6

1996-1999 513 128.2

2001 146 146

2005-2006 199 199

2006-2007 164 164

2007-2008 185 185

Source: Base de données, Service de chirurgie vasculaire HSS – CHUQ/HSFA

CHIRURGIE ÉLECTIVE AAA

Chirurgie

conventionnelle

Chirurgie par

endoprothèse

%

2005-2006 144 55 27.6

2006-2007 108 56 34.1

2007-2008 124 61 33

Séjour moyen Chirurgie

conventionnelle

Chirurgie par

endoprothèse

2006-2007 14.35 jours 6.43 jours

2007-2008 13.16 jours 5.96 jours

CHUQ, Med Écho

An infrarenal aortic aneurysm.

The Crawford classification of thoracoabdominal aortic aneurysms is defined by anatomic location and the extent of

involvement. Type I aneurysms involve all or most of the descending thoracic aorta and the upper abdominal aorta; type II

aneurysms involve all or most of the descending thoracic aorta and all or most of the abdominal aorta; type III aneurysms

involve the lower portion of the descending thoracic aorta and most of the abdominal aorta; and type IV aneurysms

involve all or most of the abdominal aorta, including the visceral segment. (Adapted from Crawford ES: Thoracoabdominal

and supra-renal abdominal aortic aneurysm. In Ernst CB, Stanley JC [eds]: Current Therapy in Vascular Surgery.

Philadelphia, Decker, 1987, pp 96-98.)

Downloaded from: Miller's Anesthesia (on 25 February 2009 11:48 PM)© 2007 Elsevier

Facteurs modifiant la réponse:

Niveau du clampage

La durée

Maladie coronarienne

Fonction myocardique

La volémie

Les collatérales

Activation Σ ,rénine-angiotensine

Clampage: Facteurs Humoraux

Acidose

Rénine & Angiotensine

Adrénaline et nor-adrénaline

Radicaux libres

Prostaglandines

Plaquettes et neutrophiles

Myocardial depressant factor

Shift of blood volume proximally to clamp

Blood volume and

flow in muscles

proximal to clamp

Lung

blood

volume

Intracranial

blood

volume

Venous

return,

preload

Supraceliac Aox

AoX

Passive venous recoil distal to clamp

Catecholamines (and other venoconstrictors)

Active venoconstriction proximal and distal to clamp

Venous capacity

Shift of blood volume

into splanchnic

vasculature

Venous return,

preload(if splanchnic

venous tone Is high)

Infraceliac Aox

Venous return,

preload(if splanchnic

venous tone Is low)

Systemic hemodynamic response to aortic cross-clamping. Preload (asterisk) does not necessarily increase with infrarenal

clamping. Depending on splanchnic vascular tone, blood volume can be shifted into the splanchnic circulation, and preload

does not increase. Ao, aortic; AoX, aortic cross-clamping; R art, arterial resistance. (Adapted from Gelman S: The

pathophysiology of aortic cross-clamping and unclamping. Anesthesiology 82:1026-1060, 1995.)

Downloaded from: Miller's Anesthesia (on 25 February 2009 11:48 PM)© 2007 Elsevier

AoX

Passive recoil distal to clamp Catecholamines

(and other vasoconstrictors) Impedance to Ao flow

If coronary flow and

contractility increase

If coronary flow and

contractility do not increase

Coronary flow

Contractility

CO

© Elsevier Science 2005

Active venoconstriction

proximal and distal to clamp R art

Preload* Afterload

Systemic hemodynamic response to

aortic unclamping. AoX, aortic cross-

clamping; Cven, venous capacitance;

R art, arterial resistance; Rpv,

pulmonary vascular resistance. (From

Gelman S: The pathophysiology of

aortic cross-clamping and unclamping.

Anesthesiology 82:1026-1060, 1995.)Downloaded from: Miller's Anesthesia

(on 25 February 2009 11:48 PM)

© 2007 Elsevier

© Elsevier Science 2005

AoX

Distal tissue Ischemia "Mediators" release

Distal vasodilation Cven Permeability(by end of clamping period)

R art

UNCLAMPING

Myocardial

contractility"Mediators" production

and washout

Pulmonary

edema

Rpv

Central hypovolemia

Venous return

Distal shift of blood volume Loss of intravascular fluid

Cardiac output

Hypotension

Spinal cord perfusion

pressure and flow (SNP+)

Ao proximal

pressure (SNP-)Shift of blood

volume to the brainAo distal,

pressure (SNP+)

ICP (SNP+)

AoX (Thoracic)

EFFECT OF LEVEL OF AORTIC OCCLUSION ON

CHANGES IN CARDIOVASCULAR VARIABLES

Cardiovascular Variable Supraceliac

% Change in variable, by level of aortic Occlusion

Suprarenal-

InfracellacInfrarenal

Mean arterial blood pressure

Pulmonary capillary wedge pressure

End-diastolic area

End-systolic area

Ejection fraction

Abnormal motion of wall, % of patients

New myocardial infarctions, % of patients

54

38

28

69

-38

92

8

5a

10a

2a

10a

-10a

33

0

aStatistically different (P < .05) from group undergoing supraceliac aortic occlusion. Adapted with

permission from Roizen MF, Ellis JE, Foss JF et al: Intraoperative management of the patient requiring

supraceliac aortic occlusion. In Veith FJ, Hobson RW. Williams RA, Wilson SE (eds): Vascular Surgery,

2nd ed, p 256. New York, McGraw-Hili, 1994.

2a

0a

9a

11a

-3a

0

0

PHYSIOLOGIC CHANGES AND THERAPEUTIC INTERVENTIONS

WITH AORTIC CROSS-CLAMPING*

Hemodynamic Changes Arterial blood pressure

Segmental wall motion abnormalities

Left ventricular wall tension

Ejection fraction

Cardiac output†

Renal blood flow

Pulmonary occlusion pressure

Central venous pressure

Coronary blood flow

Metabolic Changes

Total body oxygen consumption

Total body carbon dioxide production

Mixed venous oxygen saturation

Total body oxygen extraction

Epinephrine and norepinephrine

Respiratory alkalosis

Metabolic acidosis

Therapeutic Interventions

Afterload reduction

Sodium nitroprusside

Inhalational anesthetics

Amrinone

Shunts and aorta-to-femoral bypass

Preload reduction

Nitroglycerin

Controlled phlebotomy

Atrial-to-femoral bypass

Renal protection

Fluid administration

Distal aortic perfusion techniques

Mannitol

Drugs to augment renal perfusion

Other changes

Hypothermia

Minute venti!ation

Sodium bicarbonate

*These changes are of greater significance with longer duration of cross-clamping and with more proximal cross-clamping. † Cardiac output may increase with thoracic cross-clamping.‡ When ventilatory settings are unchanged from preclamp levels.

PHYSIOLOGIC CHANGES AND THERAPEUTIC INTERVENTIONS

WITH AORTIC UNCLAMPING*

Hemodynamic Changes Myocardial contractility

Arterial blood pressure

Pulmonary artery pressure

Central venous pressure

Venous return

Cardiac output

Metabolic Changes

Total-body oxygen consumption

Lactate

Mixed venous oxygen saturation

Prostaglandins

Activated complement

Myocardial-depressant factors

Temperature

Metabolic acidosis

Therapeutic Interventions Inhaled anesthetics

Vasodilators

Fluid administration

Vasoconstrictor drugs

Reapply cross-clamp for severe

hypotension

Consider mannitol

Consider sodium bicarbonate

*These changes are of greater significance with longer duration of cross-clamping and

with more proximal cross-clamping.

Clampage: Effets sur les organes

Poumons: > résistance, > PAP , > perméabilité

Reins: NTA, < flot cortical

Intestins: ischémie, nécrose

Moelle: paraplégie

Renal Hemodynamic and Functional

Changes Produced by Infrarenal Aortic

Cross-Clamping and Declamping

Variable

Urinary output (mL/min)51Cr EDT A clearance (mL/min)

Renal blood flow (mL/min)

Filtration fraction

Renal vascular resistance

(dyn · sec · cm-5)

Preclamp

4.45 ± 3.42

90 ± 27

1,034 ± 254

0.22 ± 0.06

7,901 ± 2,617

Preclamp

3.10 ± 1.58

71 ± 18

622 ± 135‡

0.25 ± 0.06

13,517 ± 4,144*

Postclamp

3.03 ± 1.69

71 ± 30

566 ± 226‡

0.27 ± 0.06

14,884 ± 6,124†

(X ± SO, n = 12).

Statistical difference from preclamp data: *P < 0.05, †p < 0.01, ‡p < 0.001.

Adapted from Gamulin Z, Forster A, Morel 0, et al: Anesthesiology 61:394, 1984.

Complications rénales: prévention

↓ durée clampage

Conserver perfusion rénale (volémie,débit)

↓ métabolisme (perfusion rénale froide,

furosémide,hypothermie systémique)

↓ insulte de re-perfusion ( mannitol )

Modification flot rénal ( dopamine,

mannitol,furosémide,fenoldopam)

Cross section of a human torso showing the origin of the anterior spinal artery (ASA) from

cervical radicular arteries. The ASA, through its course to the conus, receives additional

blood from medullary arteries that derive from intercostals off the aorta. The majority of these

arteries arise from the thoracic aorta. Any time the thoracic aorta is cross-clamped, the

spinal cord is at risk of ischemia leading to the development of paraplegia postoperatively.

Drain Lombaire

PPM = PAM – PLCR

Hypothèse : PAM = Pression au niveau

artère spinale antérieure !!!!

Pression sous le clampage ~ 20 mmg

Avec ou sans CEC ?

Pour ↑ PPM = ↑ PAM ou ↓ PLCR

Drain Lombaire

Controverse

Etudes animales

Pression ≠ débit

Clampage = ↑ pression LCR ?

Chez l’humain ↑ pression → ↑ réabsorption

NNT ?

Complications possibles

Coselli, et al.

Safi, et al.

An approach to spinal cord protection during

descending or thoracoabdominal aortic repairsLars G Svensson (ATS 1999;67;1935-6)

METHODS OF SPINAL CORD PROTECTION DURING

DESCENDING THORACIC AORTIC SURGERY170

Limitation of cross-clamp duration Distal circulatory support Reattachment of critical intercostal arteries CSF drainage Hypothermia

- Moderate systemic (32-34°C)- Epidural cooling- Circulatory arrest

Maintenance of proximal blood pressure - Pharmacotherapy

Systemic: Corticosteroids, barbiturates, naloxone, calcium channel antagonists, O2 free radical scavengers, NMDA antagonists, mannitol, magnesium, vasodilators (adenosine papaverine, prostacyclin), perfluorocarbons, colchicine

Intrathecal: Papaverine, magnesium, tetracaine, perfluorocarbons

Avoidance of postoperative hypotension Sequential aortic clamping Enhanced monitoring for spinal cord ischemia

- Somatosensory-evoked potentials - Motor-evoked potentials- Hydrogen-saturated saline- Avoidance of hyperglycemia

CSF, cerebrospinal fluid; NMDA, N-methyl-D-aspartate.

Improved survival after introduction of an emergency endovascular

therapy protocol for ruptured abdominal aortic aneurysms

Randy Moore, MD, FRCSC,a Mark Nutley, MD, FRCSC,a Claudio S. Cina, MD, FRCSC,b Mona Motamedi, BA,a Peter

Faris, PhD,c and Wesam Abuznadah, MD,a Calgary, Alberta, and Hamilton,Ontario, Canada

(J Vasc Surg 2007;45:443-50.)

Emergency Ruptured AAA Repair Algorithm:

Ruptured AAA

EVAR Available EVAR Not Available

*permissive hypotension:

a state of consciousness

with a systolic

blood pressure >90 mm Hg

Not Endovasvular

Candidate

Permissive*

Hypotension OR

Angiogram

EVAR if Candidate

StableUnstable

≤ 80mmHg

Spiral CTA

Unstable

≤ 80mmHg

Permissive*

Hypotension

Spiral CTA OR

Open Repair

Stable

occluder