UBP 3.6 (Short Form): Cardiovascular – Thoracic Aortic Disection

Question 1

What are your perioperative concerns in providing anesthesia for this case?

(A 62-year-old, 87 kg, male presents for open repair of a dissecting aneurysm in the descending thoracic aorta. A 3/6 early diastolic, high-pitched murmur is heard over the left sternal border. His history includes 45 years of tobacco use, hypertension, diabetes, severe GERD, and the placement of a drug-eluting coronary stent three months ago. His medications include atenolol, hydrochlorothiazide, simvastatin, aspirin, and sublingual nitroglycerine. Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 ºC, Hct = 32)

Answer 1

My primary concerns in managing this patient include the risk for:

1. aneurysmal rupture;
2. propagation of the aneurysm
   
   • (potentially leading to aortic insufficiency and/or cardiac tamponade),
3. myocardial ischemia/infarction
   
   • (secondary to coronary artery disease, hypertension, recent stent placement, likely aortic regurgitation, possible aneurysmal involvement with the coronary arteries, perioperative hemodynamic instability, cross-clamp application, and potential massive blood loss);
4. post-operative respiratory complications
   
   • (secondary to long-term tobacco abuse, one-lung ventilation, and surgical manipulation of the diaphragm and lungs);
5. paraplegia
   
   • (secondary to aneurysmal/surgical disruption of radicular arteries supplying the anterior spinal cord, cross-clamp application, hemodynamic instability, potential massive blood loss, and hyperglycemia secondary to diabetes mellitus);
6. post-operative acute kidney injury
   
   • (secondary to cross-clamp application, diabetes mellitus, aneurysmal/surgical disruption of the renal arteries, hemodynamic instability, and potential massive blood loss);
7. visceral/mesenteric injury
   
   • (secondary to cross-clamp application, hemodynamic instability, anemia, and aneurysmal/surgical disruption of the superior/inferior mesenteric arteries and/or the celiac trunk)
8. stroke
   
   • (secondary to aneurysmal/surgical disruption of the left common carotid or innominate arteries, embolization of air or thrombotic material, hypertension, hemodynamic instability, and cross-clamp application);
9. difficult airway management
   
   • (secondary to possibly aneurysmal compression of the trachea, lung parenchyma, or superior vena cava → tracheal deviation, rapid desaturation, and airway edema;
   • diabetes mellitus → possible diabetic stiff joint syndrome;
   • double-lumen tube placement;
   • GERD; and
   • large fluid shifts → possible post-operative airway edema);
10. hemorrhage (secondary to aneurysm rupture, surgical trauma, coagulopathy, heparinization, hypothermia, and acidosis); and
11. congestive heart failure (secondary to myocardial ischemia; likely aortic regurgitation; and overaggressive fluid administration).

Question 2

What is the DeBakey classification of aortic dissection? Is it important?

(A 62-year-old, 87 kg, male presents for open repair of a dissecting aneurysm in the descending thoracic aorta. A 3/6 early diastolic, high-pitched murmur is heard over the left sternal border. His history includes 45 years of tobacco use, hypertension, diabetes, severe GERD, and the placement of a drug-eluting coronary stent three months ago. His medications include atenolol, hydrochlorothiazide, simvastatin, aspirin, and sublingual nitroglycerine. Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 ºC, Hct = 32)

Answer 2

Due to the strong correlation between clinical outcome and the extent of aortic dissection, several classification systems, such as the DeBakey, Stanford, and Crawford systems, have been developed.

The DeBakey classification system defines type I dissections as originating in the ascending aorta and extending distally to involve the descending aorta (thoracic and/or abdominal aorta).

Type II dissections originate in the ascending aorta and do NOT extend beyond the innominate artery.

Type III dissections originate beyond the left subclavian artery and extend distally to the diaphragm (type IIIA), or the aorto-iliac bifurcation (type IIIB).

Acute aortic dissection involving the ascending aorta (DeBakey type I and II) is a surgical emergency, requiring immediate surgical repair.

Whereas, acute dissection involving the descending aorta (DeBakey type III), is most often treated medically with blood pressure and pain control.

However, type III dissections may require surgical intervention if they develop significant aneurysmal dilatation, are at risk of impending rupture, or result in end-organ ischemia.

Clinical Notes:

• Anatomic Division of the Aorta
  
  • Ascending Aorta – between the aortic valve and the innominate artery
  • Aortic Arch – between the innominate and the left subclavian artery
  • Descending thoracic aorta – between the left subclavian and the diaphragm
  • Abdominal aorta – below the diaphragm
• Stanford Classification
  
  • Type A
    
    • Involvement of the ascending aorta with or without involvement of the arch or descending aorta
    • Includes DeBakey Types I and II
    • More common than Type B
  • Type B
    
    • All cases in which the ascending aorta is not involved
    • Includes DeBakey Types IIIa and IIIb
• Crawford Classification System of Thoracoabdominal Aortic Aneurysms (See Practice Set #5.8)
  
  • Type I
    
    • Originates below the left subclavian artery and extends into the abdominal aorta, including the celiac axis and mesenteric arteries
  • Type II
    
    • Involves the same area as Type I, with extension caudally to include the infrarenal abdominal aorta
  • Type III
    
    • Originates in the lower descending thoracic aorta (below the 6th rib) and involves the remainder of the aorta (the origin is lower in the descending thoracic aorta than with Type I or Type II)
  • Type IV
    
    • Originates at the diaphragm and involves the abdominal aorta only
  • Type V
    
    • Originates below the 6th rib (lower thoracic aorta) and extends to the renal arteries

Question 3

What is the significance of his diastolic murmur?

(A 62-year-old, 87 kg, male presents for open repair of a dissecting aneurysm in the descending thoracic aorta. A 3/6 early diastolic, high-pitched murmur is heard over the left sternal border. His history includes 45 years of tobacco use, hypertension, diabetes, severe GERD, and the placement of a drug-eluting coronary stent three months ago. His medications include atenolol, hydrochlorothiazide, simvastatin, aspirin, and sublingual nitroglycerine. Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 ºC, Hct = 32)

Answer 3

This diastolic murmur could represent a previous cardiac condition or propagation of the aortic dissection into the aortic valve with resultant aortic regurgitation.

Acute aortic regurgitation –

• produces volume overload of the left ventricle due to added regurgitant volume;
• reduces the effective forward stroke volume;
• may result in pulmonary edema due to rapidly increasing left ventricular end-diastolic pressures;
• increases myocardial oxygen demand; and
• results in reduced myocardial blood supply secondary to reduced diastolic pressures in the aorta and/or increased ventricular end-diastolic pressures.

As a result of these factors, myocardial ischemia may occur even in the absence of coronary artery disease.

In the case of aortic valve insufficiency,

bradycardia should be avoided, since increased diastolic time leads to increased regurgitant volume and worsening cardiac function.

Question 4

A family member tells you that the patient had rheumatic fever as a child, and has lived with a leaky aortic valve for years. Would you continue his B-blocker?

(A 62-year-old, 87 kg, male presents for open repair of a dissecting aneurysm in the descending thoracic aorta. A 3/6 early diastolic, high-pitched murmur is heard over the left sternal border. His history includes 45 years of tobacco use, hypertension, diabetes, severe GERD, and the placement of a drug-eluting coronary stent three months ago. His medications include atenolol, hydrochlorothiazide, simvastatin, aspirin, and sublingual nitroglycerine. Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 ºC, Hct = 32)

Answer 4

I would continue his B-blocker therapy for two reasons:

first, the preoperative discontinuation of B-blocker therapy is associated with an increased risk of myocardial ischemia and chest pain;

second, it is important to control his heart rate and blood pressure in order to avoid propagation and/or rupture of his aortic dissection (decreasing blood pressure and the force of ventricular contraction reduces aortic wall stress by reducing shear pressure or dP/dT*).

Before administering additional B-blocker (beyond his normal dose), however, I would correct any factors that may be contributing to his tachycardia and hypertension, such as pain, hypovolemia, infection, or anemia.

If this failed to resolve the problem, I would consider starting an infusion of a short acting, titratable, B-blocker such as esmolol, followed by nitroprusside.

My treatment goals would be –

• to reduce intramural pressures and aortic shear forces that could lead to propagation or rupture of the dissection;
• reduce regurgitant volumes by reducing left ventricular afterload; and,
• at the same time, avoid bradycardia, which could increase aortic regurgitation by increasing diastolic time.

Additionally, perioperative B-blockers have been shown to reduce the perioperative and long-term cardiac morbidity/mortality associated with high-risk vascular surgery.

Moreover, I would start the esmolol infusion prior to giving nitroprusside, since the administration of a vasodilator prior to adequate B-blocker could lead to increased aortic wall stress.

The advantage of a short acting agent, like esmolol, is that it would allow me to quickly adjust dosing to fit a rapidly changing clinical situation (i.e. reduce or discontinue infusion if bradycardia developed).

Clinical Note:

• *dP/dT = the change in blood pressure / change in time
• Beta-blockers should be continued in patients undergoing surgery who are currently taking beta-blockers for treatment of indicated conditions (Class I).
  
  • 2009 ACCF/AHA Focused Update on Perioperative Beta Blockade

Question 5

Would you initiate B-blocker therapy if he were not already taking a B-blocker?

(A 62-year-old, 87 kg, male presents for open repair of a dissecting aneurysm in the descending thoracic aorta. A 3/6 early diastolic, high-pitched murmur is heard over the left sternal border. His history includes 45 years of tobacco use, hypertension, diabetes, severe GERD, and the placement of a drug-eluting coronary stent three months ago. His medications include atenolol, hydrochlorothiazide, simvastatin, aspirin, and sublingual nitroglycerine. Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 ºC, Hct = 32)

Answer 5

I would NOT initiate high-dose, untitrated, B-blocker therapy to a patient not currently taking B-blockers unless it was absolutely necessary.

While this intervention may reduce the risk of aneurysm rupture, aneurysm propagation, and the patient’s cardiovascular morbidity and mortality, it would also increase the incidence of hypotension, bradycardia, and stroke, along with an overall increase in mortality.

Rather, if given the opportunity, I would initiate B-blocker therapy at least 7-10 days prior to surgery, and carefully titrate dosing to achieve a heart rate 60-80 beats/minute while avoiding significant bradycardia and/or hypotension.

• Clinical Note:*
• In patients undergoing noncardiac surgery who are not currently taking beta-blockers, routine administration of high-dose, untitrated perioperative beta-blockers is NOT recommended (ACCF/AHA Class III Recommendation).

Question 6

How would you evaluate his pulmonary status?

(A 62-year-old, 87 kg, male presents for open repair of a dissecting aneurysm in the descending thoracic aorta. A 3/6 early diastolic, high-pitched murmur is heard over the left sternal border. His history includes 45 years of tobacco use, hypertension, diabetes, severe GERD, and the placement of a drug-eluting coronary stent three months ago. His medications include atenolol, hydrochlorothiazide, simvastatin, aspirin, and sublingual nitroglycerine. Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 ºC, Hct = 32)

Answer 6

Recognizing that aortic repair is associated with a high incidence of postoperative respiratory failure (25-45%), I would:

1. order a chest-xray to aid in identifying any pulmonary disease or underlying infection;
2. perform a physical exam to identify any signs and symptoms consistent with COPD, such as cough and sputum production; and
3. obtain any relevant history, such as frequency of pulmonary infections, frequency and severity of exacerbations, exercise tolerance, and number and course of hospitalizations, and efficacy of past treatments.
   
   • If the patient were minimally symptomatic, exhibited good functional status, and did not show any signs of an acute pulmonary process on chest x-ray, I would not pursue further pulmonary testing.
   • However, if the patient exhibited signs and symptoms consistent with significant pulmonary disease or showed an acute pulmonary process on chest x-ray, I would obtain – (see next #4 step)
4. an ABG to better assess ventilation and oxygenation;
5. an ECG to identify any signs of pulmonary hypertension (i.e. narrowly split heart sound, a loud second heart sound secondary to pulmonic valve closure, and right ventricular and/or atrial hypertrophy); and
6. pulmonary function tests to better evaluate the severity of his COPD, determine his response to bronchodilator therapy, predict his tolerance of one-lung ventilation, and assess his risk for postoperative pulmonary complications.

Clinical Note:

• PFT results consistent with an increased risk for postoperative mechanical ventilation include:
  
  • FEV 1 < 2 L total
  • Maximum breathing capacity < 50% of predicted
  • MMEFR < 50% of predicted

Question 7

Would you place a lumbar drain?

(A 62-year-old, 87 kg, male presents for open repair of a dissecting aneurysm in the descending thoracic aorta. A 3/6 early diastolic, high-pitched murmur is heard over the left sternal border. His history includes 45 years of tobacco use, hypertension, diabetes, severe GERD, and the placement of a drug-eluting coronary stent three months ago. His medications include atenolol, hydrochlorothiazide, simvastatin, aspirin, and sublingual nitroglycerine. Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 ºC, Hct = 32)

Answer 7

Assuming that this patient with a drug-eluting stent had discontinued any thienopyridine therapy for the appropriate interval (clopidogrel = 7 days; ticlopidine = 14 days) and exhibited no signs of coagulopathy or other contraindication, I would consider placing a lumbar drain.

Placement would allow for passive drainage of CSF to a pressure of 8-10 mmHg during the procedure and postoperatively (for about 48 hours) to better preserve adequate spinal cord perfusion.

Perfusion pressure to the spinal cord is defined as the mean distal aortic pressure minus the CSF pressure or central venous pressure (whichever is highest).

While spinal cord blood flow is controlled by autoregulation (between pressures of 50-125 mmHg), the potential for impaired autoregulation, combined with clamp-induced increases in CSF pressure (hyperemia above the proximal clamp → increased ICP → redistribution of CSF into the intrathecal space → increase in CSF pressure by 10-15 mmHg), make the careful drainage of CSF a reasonable strategy to improve spinal cord perfusion (Class I recommendation for spinal cord protection for patients at high risk for neurologic injury).

However, there are potential complications associated with CSF drainage, including – spinal/epidural hematoma, headache, intracranial bleeding (secondary to tearing of cerebral bridging vessels), meningitis, and chronic CSF leakage.

• Clinical Note:*
• When draining CSF to a specific target, be sure that the zero point of the transducer is set at the patient’s mid-axillary line or external auditory meatus while the patient is in the supine position.

Question 8

You are planning to place the lumbar drain and an epidural catheter for pain management.

Upon further inquiry, you learn that the patient did discontinue his clopidogrel seven days ago, but was started three days ago on eptifibatide (integrilin) and intravenous heparin.

Would you still proceed with the placement of these neuraxial catheters?

(A 62-year-old, 87 kg, male presents for open repair of a dissecting aneurysm in the descending thoracic aorta. A 3/6 early diastolic, high-pitched murmur is heard over the left sternal border. His history includes 45 years of tobacco use, hypertension, diabetes, severe GERD, and the placement of a drug-eluting coronary stent three months ago. His medications include atenolol, hydrochlorothiazide, simvastatin, aspirin, and sublingual nitroglycerine. Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 ºC, Hct = 32)

Answer 8

I would still proceed with lumbar drain placement as long as –

• he had discontinued his eptifibatide and intravenous heparin for at least 4 hours,
• he had a normal PTT
  
  • (heparin activity would prolong the PTT), and
• there were no signs of coagulopathy
  
  • (the ASRA recommendation is to delay neuraxial placement for 4-8 hours following the discontinuation of eptifibatide and 2-4 hours following the discontinuation of intravenous heparin).

Platelet GP IIb/IIIa inhibitors are sometimes used for “bridging therapy” when a patient who requires thienopyridine therapy to prevent stent thrombosis must undergo a surgical procedure where the risk of bleeding makes the continuation of a long-acting platelet inhibitor unacceptable.

When the decision is made to employ bridging therapy, a typical strategy would be to:

1. discontinue the thienopyridine 5-7 days prior to surgery
   
   • (7 days would be required if planning to place an epidural catheter or lumbar drain),
2. continue aspirin throughout the perioperative period,
3. start a short-acting platelet inhibitor, such as eptifibatide or tirofiban, 2-3 days before surgery,
4. consider starting a concomitant heparin infusion, and
5. discontinue any “bridging” drugs 6 hours prior to surgery
   
   • (the aspirin should be continued, if possible).

• Clinical Note:*
• Heparin alone is insufficient to prevent stent thrombosis because the heparin anti-thrombin complex’s ability to inactivate fibrin-bound thrombin and factor Xa is limited.

Question 9

The surgeon tells you he is planning to utilize left-heart bypass with a pump, oxygenator, and heat exchanger during the procedure.

Would you still place the lumbar drain?

(A 62-year-old, 87 kg, male presents for open repair of a dissecting aneurysm in the descending thoracic aorta. A 3/6 early diastolic, high-pitched murmur is heard over the left sternal border. His history includes 45 years of tobacco use, hypertension, diabetes, severe GERD, and the placement of a drug-eluting coronary stent three months ago. His medications include atenolol, hydrochlorothiazide, simvastatin, aspirin, and sublingual nitroglycerine. Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 ºC, Hct = 32)

Answer 9

Even though left-heart bypass requires heparinization,

I would plan to proceed with lumbar drain placement for this patient at high risk for neurologic injury.

After discussing the risks and benefits of drain placement with the surgeon, patient, and family,

I would –

• ensure that preoperative anticoagulants had been discontinued for a sufficient period of time,
• rule out any current coagulopathy,
• delay systemic heparinization for 60 minutes following placement of the lumbar drain,
• utilize the smallest amount of heparin necessary to achieve therapeutic objectives (partial bypass usually requires about 100 U/kg),
• monitor the patient carefully for any signs of spinal or epidural hematoma, and
• ensure adequate coagulation at the time of catheter removal.

In the case of traumatic placement, a delay of surgery for 24 hours would be desirable to reduce the risk of spinal/epidural hematoma (there is no evidence to support this practice; ASRA recommends a delay when utilizing full heparinization, but does not make a recommendation when planning low dose systemic heparinization – i.e. 100 U/kg).

However, the urgency of this case may preclude such a delay, making it esential that post-operative precautions be taken to avoid an undetected epidural or subdural hematoma.

To this end, I would ensure normal coagulation prior to removal of the lumbar drain and order neurological examinations every hour to detect the first signs of spinal cord compression secondary to hematoma formation.

If an epidural catheter were in place for post-operative pain control, I would utilize narcotics alone or in combination with low concentration local anesthetics in order to preserve the patient’s lower extremity motor function and allow for adequate neurologic monitoring.

Question 10

The surgeon says he wishes to use MEP and SSEP monitoring for the case.

Given this information, would you place an epidural for the procedure?

(A 62-year-old, 87 kg, male presents for open repair of a dissecting aneurysm in the descending thoracic aorta. A 3/6 early diastolic, high-pitched murmur is heard over the left sternal border. His history includes 45 years of tobacco use, hypertension, diabetes, severe GERD, and the placement of a drug-eluting coronary stent three months ago. His medications include atenolol, hydrochlorothiazide, simvastatin, aspirin, and sublingual nitroglycerine. Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 ºC, Hct = 32)

Answer 10

Assuming there were no contraindications, I would consider placing an epidural for this case.

However, since the surgeon wishes to utilize evoked potential monitoring during the procedure, I would use only epidural narcotics during the case, reserving the epidural administration of local anesthetics for post-operative care.

In this way, I would avoid the confounding effects of local anesthetic-induced sensory and motor impairment on evoked potential signals.

Since this patient will require systemic heparinization, I would rule out any current coagulopathy, delay systemic heparinization for 60 minutes following placement, minimize heparin dosing, and plan to remove the epidural only after the complete restoration of motor function (to avoid diagnostic confusion) and normal coagulation.

While the use of epidural analgesia has not been definitively proven to reduce the incidence of cardiovascular, pulmonary, or renal complications, it does provide excellent post-operative pain control and may result in – improved respiratory function (decreased incidence of atelectasis, pulmonary infections, respiratory failure, and prolonged mechanical ventilation), improved gastrointestinal motility, improved graft patency (reduced coagulation response), and reduced incidence of postoperative myocardial ischemia (secondary to an attenuation of the stress response and, when a thoracic epidural is used, coronary artery dilation).

However, there are risks associated with placement such as – epidural hematoma, sympatholysis-induced hypotension, epidural abscess, headache, meningitis, and interference with spinal cord monitoring and/or postoperative neurological exam.

Question 11

You are appropriately concerned about the potential for massive blood loss.

Recognizing this risk, what would you do?

(A 62-year-old, 87 kg, male presents for open repair of a dissecting aneurysm in the descending thoracic aorta. A 3/6 early diastolic, high-pitched murmur is heard over the left sternal border. His history includes 45 years of tobacco use, hypertension, diabetes, severe GERD, and the placement of a drug-eluting coronary stent three months ago. His medications include atenolol, hydrochlorothiazide, simvastatin, aspirin, and sublingual nitroglycerine. Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 ºC, Hct = 32)

Answer 11

Recognizing the potential for massive blood loss during the procedure, I would:

1. place at least two large-bore intravenous lines (in addition to a large-bore central introducer);
2. ensure that rapid transfusing and blood warming devices were in the room;
3. have 10-15 units of PRBCs and 5 units of FFP in the operating room (1 unit of FFP should be available for every 1-2 units of PRBCs) with additional units available in the blood bank; and
4. plan to utilize intraoperative cell salvage.

Moreover, I would have a discussion with the surgeon concerning the risks and benefits of additional blood conservation strategies, such as – acute normovolemic hemodilution and/or the administration of an antifibrinolytic, such as Σ-aminocaproic acid or tranexamic acid.

Question 12

The surgeon wants to employ acute normovolemic hemodilution (ANH).

Would you agree?

(A 62-year-old, 87 kg, male presents for open repair of a dissecting aneurysm in the descending thoracic aorta. A 3/6 early diastolic, high-pitched murmur is heard over the left sternal border. His history includes 45 years of tobacco use, hypertension, diabetes, severe GERD, and the placement of a drug-eluting coronary stent three months ago. His medications include atenolol, hydrochlorothiazide, simvastatin, aspirin, and sublingual nitroglycerine. Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 ºC, Hct = 32)

Answer 12

Assuming the patient’s hematocrit was >/= 33%, his hemoglobin was >/= 11 g/dL, his smoking has not led to severe pulmonary disease, and there is no significant renal impairment (possibly secondary to diabetes and/or hypertension),

I would agree to utilize acute normovolemic hemodilution as a blood conservation strategy recognizing that avoiding exposure to allogeneic blood transfusion reduces the risk of infection, transfusion reactions, and red cell alloimmunization.

The rationale for ANH is that blood loss is minimized by reducing the hematocrit of blood likely to be shed during the procedure (i.e. normovolemic hemodilution).

Autologous blood collected at the beginning of the case prior to hemodilution (higher hematocrit) is then re-infused when significant bleeding has been controlled.

Unfortunatley, this strategy has only been shown to be of moderate benefit, saving the equivalent of 1-2 units of PRBCs even when the patient’s initial hematocrit is very high and intraoperative blood loss is substantial (> 70% of the patient’s blood volume).

In this case, his cardiac disease may limit the reduction in initial hematocrit, further limiting the benefits of this approach.

Clinical Note:

• Ischemic cardiac disease is not necessarily a contraindication to ANH, but the initial reduction in hematocrit should be limited in order to avoid end-organ ischemia.
• CONTRAINDICATIONS to ANH:
  
  • Anemia (initial hematocrit is < 33 % or the hemoglobin is < 11 g/dL)
  • Impaired renal function – the patient may be unable to excrete the fluid load associated with normovolemic hemodilution
  • Conditions that would make an increase in cardiac output undesirable, such as aortic stenosis
  • Significant pulmonary disease – oxygen delivery to tissues may be inadequate in the setting of significant pulmonary disease and the decreased oxygen content associated with ANH
  • Pre-existing coagulopathy

Question 13

Describe how you would perform acute normovolemic hemodilution.

(A 62-year-old, 87 kg, male presents for open repair of a dissecting aneurysm in the descending thoracic aorta. A 3/6 early diastolic, high-pitched murmur is heard over the left sternal border. His history includes 45 years of tobacco use, hypertension, diabetes, severe GERD, and the placement of a drug-eluting coronary stent three months ago. His medications include atenolol, hydrochlorothiazide, simvastatin, aspirin, and sublingual nitroglycerine. Vital Signs: HR = 106, BP = 152/85 mmHg, RR = 24, T = 37 ºC, Hct = 32)

Answer 13

After ensuring the patient was a good candidate for ANH, I would –

collect 1-2 units of his blood, while simultaneously administering warmed crystalloids or colloids to maintain normovolemia.

Given this patient’s coronary artery disease, I would only allow his hematocrit to be reduced to around 27% with the initial withdrawal (may use the “estimated allowable blood loss” calculation to approximate the amount of blood to withdraw).

Then, following the cessation of significant blood loss (or earlier if clinically indicated), I would re-infuse the autologous blood in reverse order of collection, recognizing that the first unit collected contains the highest concentration of coagulation factors and platelets (re-infusion in reverse order of collection is only advantageous if all the blood collected is to be returned to the patient).

Clinical Note:

• The reduction in RBC concentration associated with ANH decreases blood viscosity, leading to decreased peripheral vascular resistance and increased cardiac output.
• This compensatory increase in cardiac output helps to maintain adequate oxygen delivery to the tissues despite a decreased hematocrit.