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[心血管麻醉] Deep Hypothermic Circulatory Arrest (DHCA)

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发表于 2009-11-23 00:15:50 | 只看该作者 回帖奖励 |倒序浏览 |阅读模式
本帖最后由 shenxiu2 于 2009-11-23 00:37 编辑

Deep Hypothermic Circulatory Arrest (DHCA)

DHCA involves the use of systemic hypothermia ( < 18’C ) and the intentional cessation of the circulation for periods up to 60 min.The technique is used when the nature of the surgical procedure makes conventional Cardiopulmonary bypass (CPB) impractical or impossible .(Table1) DHCA produces a motionless , bloodless and cannula-free surgical field, allowing unobstructed surgical access.

Table 1 Cardiac & noncardiac indications for DHCA
Cardiac :
Repair of complex congenital cardiac anomalies.
Aortic aneurysm, rupture or dissection
Aortic Arch reconstruction

Non-cardiac:
Hepatic & renal cell carcinoma
Repair of giant cerebral aneurysms
Resection of cerebral AV malformations
Pulmonary thromboendarterectomy


By reducing cellular metabolism, hypothermia preserves high –energy phosphate stores & protects organs from short period of ischaemia.
The benefits of hypothermia have to be balanced against a significant number of potential problems & complications .

Problems associated with profound hypothermia
General—prolonged CPB
Circulation ---increased plasma viscosity , decreased RBC plasticity,vasoconstriction , impaired microcirculation , left shift of Hb O2 saturation curve, cold agglutinins may worsen regional perfusion & cause hemolysis.
Cardiac-----increased predisposition to dysrhythemias.
Cerebral----vasoconstriction,risk of cerebral hyperthermia during rewarming.
Gastrointestinal----gastric dilatation & ileus;submucosal erosion & hemorrhage.impaired hepatic thermogenesis , acute pancreatitis.
Renal---decreased GFR, Na+, water & glucose reabsorption, H+ excretion.
Metabolic---Impaired glucose metabolism & tendency to hyperglycemia,tendency to metabolic acidosis, altered pharmacokinetics & pharmacodynamics.
Coagulation---Impaired coagulation , decreased platelet count , may cause DIC.


Safe period of circulatory arrest Defined as the maximum of continuous circulatory arrest that is not complicated by significant & permanent neurological injury.In general neonates & infants tolerate longer periods of DHCA than adults. Most patients tolerate 30 minutesDHCA at 18’C , whereas only &frac34; of patients tolerate 45 minutes DHCA at this temperature.

Cerebral protection
Temperature :

Hypothermia remains the single most important mechanism of cerebral protection . DHCA at 15-20’C provides the longest safe period of circulatory arrest .The application of external ice packs to the head delays brain rewarming during DHCA.
Hemodilution :
Hypothermia-induced vasoconstriction & an increase in viscosity leads to impaired micro-circulatory flow & organ ischemia.The rationale for hemodilution during hypothermic CPB is , therefore , inprovement of the microcirculation. The optimal degree of hemodilution remains unclear . A hematocrit of <10% results in inadequate tissue oxygenation during cooling & risks tissue hypoxia during rewarming.
Acid-base management :
Cerebral vasodilatation associated with pH-stst blood –gas management improves brain cooling & ensures more homogenous cooling of deeper brain structures. pH-stat may however , induce a cerebral metabolic acidosis & increase micro-embolization secondary to increased cerebral blood flow ( CBF) . On theoretical grounds, switching from pH-stst to Alpha-stat blood –gas management after cooling & prior to the onset of DHCA ( the so-called “crossover ” management has some appeal.
Glucose management :
Accumulating evidence supports the notion that tight glycemic control during DHCA is associated with improved clinical outcome.
Pharmacological :Pharmacological protection from cerebral ischemia remains elusive & at present no drug is licensed for neuroprotection in cardiac surgery . Although various anesthetic agents ( thiopental . propofol & isoflurane ) can induce EEG burst suppression & profoundly decreased cerebral metabolic rate ( for oxygen) CMRO2 , their neuro protective properties remain unproven.
Surgical strategies:


  • Selective antegrade cerebral perfusion ( SACP):
  • Involves selective cannulation of the brachiocephalic , axillary or carotid arteries. Oxygenated blood is pumped via a separate arterial line at 5-10ml / kg /min as long as perfusion pressure remains < 150mmHg.
    In addition to increasing complexity and crowding , the surgical field with cannulae, SACP is accompanied by the risk of cerebral embolization. An intact circle of Willis is required when unilateral SACP is employed. A misplaced cannulae may result in inadequate cerebral perfusion while giving a false sense of security.


  • Intermittent cerebral perfusion :
  • Intermittent systemic perfusion punctuated by about 20 minutes periods of DHCA has been used as an alternative strategy to prolong the total duration of DHCA . It si suggested that intermittent reperfusion preserves neurological tissue by replenishing cerebral high- energy phosphates and removing accumulated waste products.


  • Retrograde cerebral perfusion(RCP):
  • RCP relies on the fact that cerebral veins have no valves, involves the continuous administration of cold ( 10-15’C) oxygenated blood via a SVC cannula . Blood flow to the brain is most likely to occur via the azygos veins because the internal jugular veins possess valves.The azygos vein has connections to the vertebral venous system & the venous plexus of the foramen magnum & intracranial sinuses.Massive shunting via the superficial
    the deep vein systems, including the Internal & external jugular veins , amy result in only a small fraction of the blood entering the SVC actually reaching the cerebral arteries. For this reasonthe exact levels of CBF ^ metabolic substrate delivery provided by RCP , have yet to be defined . Suggested blood flow rates for RCP are 200-300ml/min with SVC prssure < 25 mmHg. Higher pressure associated with retrograde flow may increase the potential for cerebral oedema.
  • Theoretical adveanges of RCP include : more homogenous brain cooling ; ashout of air bubbles, embolic debris and metabolic waste products; prevention of cerebral blood cell microaggregates; and delivery of O2 and metabolic substrates to the brain. The prolongation of safe DHCA that can be achieved with RCP is less than that with SACP. RCP > 60 min is a signicant predictor of permanent neurological dysfunction.

Potential problems associated with SACP & RCP during DHCA
SACP :


  • Embolization of air or plaque
  • Cannula malposition & inadequate CBF
  • Unilaterl flow requiring flow through circle of Willis to contralateral side
  • Increased complexity of surgery & crowding of the surgical field

RCP
  • Increased inracranial pressure ( ICP )
  • Cerebral edema
  • Low level of substrate supply.


Conduct of anesthesia
Most procedures requiring DHCA are complex & prolonged . Close coordination & cooperation between the anesthetist, the perfusionist and the surgeon is essential.
The risk of coagulopathy & significant hemorrhage sould prompt early discussion of likely blood product requirements with the local transfusion service.
Prior to onset of DHCA the emphasis should be on cardiovascular stability & maintenance of tissue O2 delivery. Following the onset of CPB , systemic coling proceeds in the presence of a beating heart. The onset of hypothermia induced VF signals the need for aortic cross clamp & administration of cardioplegia. The head is surrounded by icepacks during cooling.Cooling continues until a stable core temperature of 15-20’C has been achievd for at least 20 min.

The optimal site for temperature monitoring is controversial, as gradients exist between all regions of the body.Temperature monitoring at several sites is advised to ensure uniform cooling. Nasopharyngeal temperature , which follow brain temperature relatively closely, is the preferred site for monitoring brain temperature. Bladder or rectal probes are often used to monitor core temperature.

At the onset of DHCA the pump is switched off and blood is allowed to drain from the patient via the venous line and cardiotomy line to provide bloodless field. The time of onset of DHCA should be noted. As the IV administration of drugs during DHCA is at best pointless and at worst potentially dangerous , all infusions should be discontinued and any drugs for neuroprotection administered well before the pump is switched off.

Removal of the aortic cross clamp and opening the aorta to the atmosphere exposes both the coronary & cerebral arteries to the risk of air embolism. AT the end of DHCA therefore , adequate de-airing and precautions such as head-down tilt and flooding of the surgical field with crystalloid at 4’C should be undertaken. The time of termination of DHCA should be recorded.

Following a variable period of hypothermic reperfusion , slow rewarming commences with vasodilators, such as Sodium Nitroprusside , being used to promote homogenous rewarming. Rewarming may take 45-90 min or more and should not be rushed . Hyperthermia , which exacerbates neurological injury following reperfusion , must be avoided at all costs. Infusions of anesthetic agents are restarted to avoid the risk of awareness during rewarming . The metabolic acidosis that is invariably present following DHCA normally resolves with time if CPB is adequate.
Hemoconcerntration by hemofiltration is usually undertaken during rewarming to remove excess body water & reduce the risks of cerebral ischemia secondary to anemia.

Key points:

  • Hypothermia is the single most important mechanism of serebral protection during DHCA.
  • Drugs with putative neiroprotective properties are widely used prior to DHCA despite an absence of convincing evidence of efficacy.
  • Hemidilution is used to improve microcirculation.
  • The use of continuous or intermittent cerebral perfusion techniques during DHCA may prolong the safe duration of circulatory arrest.


节录自Core Topics in Cardiac Anesthesia 2004, 第五十章
By S.L Misso & A.C Knowles.


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