UBP 5.8 (Long Form): Cardiovascular – Abdominal Aortic Aneurysm Flashcards
Secondary Subject -- CAD / CHF / HTN / Epidural for Post-operative Pain Control / Cyanide Toxicity / Post-operative Renal Failure / Arterial Line / Spinal Cord Protection / Renal Preservation / Hypothermia / Difficult Airway Management
Intra-operative Management:
You learn that the patient has a history of difficult intubation.
Would you then proceed with local or neuraxial anesthesia?
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
While both local anesthesia and neuraxial anesthesia have been safely utilized for endovascular aortic aneurysm repair,
I would proceed with general anesthesia in this case.
Local anesthesia would be inappropriate given –
- the complexity of the procedure (i.e. debranching and the use of fenestrated and/or branched stent-grafts),
- the likelihood that the duration of the case would exceed 2 hours, and
- the relatively high potential for conversion to open surgery.
Neuraxial anesthesia would be acceptable in some cases, as long as there were no contraindications (i.e. coagulopathy) and the patient gave informed consent (he should be informed that heavy sedation would not be an option since periodic breath-holding is required during angiography).
However, I would not agree to neuraxial anesthesia for this procedure because –
- a “motionless” field will be required during stent deployment (a temporary cessation of blood flow in the thoracic aorta may be provided using adenosine or inducing ventricular fibrillation),
- there is a relatively high risk for conversion to open surgery (secondary to the complexity of the case), and
- his history of difficult airway management would place the patient at an unacceptable level of risk when converting to an open procedure.
Moreover, the use of neuraxial anesthesia would preclude the use of evoked potential monitoring and TEE.
Intra-operative Management:
Placing the arterial line is difficult, and the patient is becoming agitated.
The surgeon pulls you aside and asks you to place the monitor after induction.
Would you agree?
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
I would NOT agree to delay placement unless it were absolutely essential.
Given this patient’s dissecting aneurysm, CAD, chronic HTN, and history of CHF,
it would be very important to maintain stable hemodynamics during induction.
Sympathetic stimulation during laryngoscopy could lead to hypertension and tachycardia, placing this patient at increased risk for myocardial ischemia, heart failure, and propagation or rupture of the aneurysm.
On the other hand, hypotension during induction must be avoided, since patients with CAD are dependent on normal diastolic aortic pressures to provide adequate coronary perfusion.
Therefore, since the arterial line would allow me to more quickly identify and treat changes in blood pressure, I would administer some sedation to prevent sympathetic stimulation, and place a right radial arterial line prior to induction
(the arterial line should be placed on the right upper extremity, since both femoral arteries and left brachial artery are often utilized for access during the procedure.)
Intra-operative Management:
The surgeon requests a hemodynamically “still” field for endograft deployment.
What would you do?
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
Recognizing that a hemodynamically motionless field is required for endovascular repair of the proximal descending aorta,
I would –
- utilize adenosine (6-12 mg IV via a central line) to induce transient atrioventricular heart block,
- transvenous pacing (pacing at rates of 150-180 beats/minute result in decreased left ventricular preload, stroke volume, and cardiac output), or
- right atrial flow occlusion (achieved by introducing an occlusion balloon through the femoral or jugular vein into the right atrium to inflate in the inferior or superior vena cava) to cause a temporary cessation of blood flow in the thoracic aorta.
A hemodynamically still field is also required with older generation endografts
- (when not deploying in the proximal descending aorta, newer self-expanding aortic endografts only require a temporary reduction in cardiac output during stent deployment –> MAP of 60-70 mmHg and a heart rate of 50-60 beats/minute)
- and for aneurysmal repair of the aortic arch and ascending aorta.
Clinical Note:
- The rationale for inducing a “still” field is as follows:
- Once deployed, repositioning of most thoracic endografts is difficult to impossible
- The proximity of major vessels originating from the aorta to the proximal and distal landing fields of thoracic and aortic arch stent-grafts, makes stent migration or encroachment potentially catastrophic.
- The high volume of blood flow in the thoracic aorta can lead to a “windsock effect”, pulling even a perfectly deployed graft distally before complete deployment is achieved.
Intra-operative Management:
Shortly after deploying the endograft, his blood pressure drops to 58/32 mmHg.
What could be going on?
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
Since his hypotension developed shortly after device deployment,
I would first consider persistent hemodynamic effects associated with establishing a motionless field during endograft deployment (i.e. adenosine, pacing, or occlusion balloon).
However, I would also consider other potential causes such as –
- aneurysm rupture,
- surgically-induced vascular damage (as may occur when obtaining vascular access),
- allergic reaction to contrast dye or antibiotics,
- myocardial ischemia/infarction,
- acute cardiac failure,
- arrhythmia,
- tension pneumothorax (secondary to central line placement), or
- inadvertent medication administration, including epidural local anesthetics (which could result in sympathectomy).
In any case, this is a significant drop in blood pressure that should be treated aggressively.
Intra-operative Management:
The surgeon informs you that the femoral artery was dissected when introducing the vascular sheath and he wants to convert to open surgery and repair the artery using a “clamp and sew” technique (no bypass).
How would you provide renal protection during aortic aneurysm repair?
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
There are multiple strategies for providing renal protection during aortic aneurysm repair.
In the case of endovascular aortic aneurysm repair where contrast-dye is often utilized, I would:
- ensure adequate hydration (cautiously administer fluids in this patient with CHF);
- request that the surgeon utilize contrast dye that is non-ionic, low or iso-osmolar, and low in viscosity;
- ask the surgeon to utilize TEE to minimize (or even limit) the need for contrast dye;
- initiate an infusion of sodium bicarbonate; and
- administer an antioxidant, such as N-acetylcysteine (mucomyst) or ascorbic acid
- (the administration of N-acetylcysteine is not universally recommended due to insufficient evidence and risk of anaphylactoid reactions).
- Other interventions I would consider include – the avoidance of nephrotoxic drugs
- (i.e. ACE inhibitors, ASA, NSAIDs, and aminoglycosides) and
- the administration of renal protective drugs, such as –
- statins (associated with preserved renal function after requiring suprarenal aortic cross-clamping),
- mannitol (12.5 - 25 g/70 kg or 0.25 g/kg – administered before cross-clamp),
- loop diuretics (less effective than mannitol),
- low-dose dopamine (1-3 mcg/kg/min), and
- fenoldopam.
- If aortic cross-clamping became necessary during the procedure (i.e. conversion to open surgery), I would – maintain adequate intravascular volume and hemodynamic stability during the cross-clamp period
- (maintenance of intravascular volume reduces the requirement for active reabsorption of salt and water in the kidneys, thereby reducing medullary oxygen requirements, ischemia, and perioperative renal dysfunction),
- ask the surgeon to minimize cross-clamp time, and consider:
- preconditioning, with intermittent cross-clamping of the internal iliac arteries prior to aortic cross-clamping;
- distal aortic perfusion; and
- systemic and/or regional hypothermia (the latter may be achieved with direct instillation of renal preservation fluid into the renal artery using cold LR at 4 degrees Celsius).
Clinical Notes:
- Mannitor increases renal cortical blood flow, is a free radical scavenger, increases renal prostaglandin synthesis, decreases renin secretion, and reduces ischemia-induced cellular edema.
- Loop diuretics and dopamine may provide protection through increased renal blood flow and increased urine output.
- Fenoldopam is a selective dopamine agonist that preferentially dilates the renal and splanchnic vasculature.
- Unfortunately, there is little evidence that these medications improve outcome following aortic surgery.
Intra-operative Management:
Would renal protective strategies be necessary if the proximal aortic cross-clamp is infrarenal?
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
Yes.
Even when aortic clamping occurs below the renal arteries, aortic-cross clamping results in decrease in renal blood flow (up to 40% secondary to alterations of the renin-angiotensin system and vasoconstriction) and a deleterious redistribution of intra-renal blood flow to the cortex.
Other contributing factors include surgical trauma to the renal arteries and the embolization of atherosclerosis debris to the kidneys.
Clinical Notes:
- Adequacy of renal perfusion cannot be assumed by urine output.
- Suprarenal cross-clamp application reduces renal blood flow up to 80-90%, while infrarenal cross-clamp application reduces renal blood flow up to 40%
- Acute tubular necrosis accounts for nearly all the renal dysfunction and failure that occurs after aortic reconstruction.
Intra-operative Management:
A supraceliac aortic-cross clamp is placed as planned. What are the physiologic effects associated with application of an aortic cross-clamp?
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
The cardiovascular response to aortic cross-clamping is variable, depending on –
- cross-clamp positioning
- (higher the cross-clamp application is associated with more significant changes – these changes are minimal with infrarenal cross-clamp application),
- the duration of cross-clamp application,
- the volume status of the patient,
- left ventricular function, and
- the use of distal bypass.
In general, the hemodynamic changes associated with aortic cross-clamping include –
- decreased ejection fraction,
- cardiac output
- (may stay the same or increase with thoracic cross-clamp application due to increased preload),
- renal blood flow, and
- distal perfusion pressure.
Increased afterload proximal to the clamp along with increased catecholamine release can lead to increases in –
- arterial blood pressure,
- left ventricular wall tension,
- central venous pressure, and
- pulmonary occlusion pressure.
Metabolic changes associated with aortic cross-clamping include –
- increased mixed venous oxygen saturation,
- increased catecholamine release (epinephrine and norepinephrine),
- decreased total body oxygen consumption, and
- metabolic acidosis.
Finally, thoracic cross-clamp application results in – increased CSF pressure
- (increased systemic pressure proximal to the clamp results in redistribution of blood volume to the intracranial compartment with subsequent redistribution of CSF into the spinal fluid space, which then increases intrathecal CSF pressure).
These changes increase the risk for – myocardial ischemia and heart failure as well as distal organ ischemia.
With infrarenal aortic clamping, the cardiovascular effects become less pronounced.
Intra-operative Management:
The surgeon suggests allowing the patient to become hypothermic. Would you agree?
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
While there are some risks, such as cardiac arrhythmias (atrial or ventricular fibrillation), myocardial depression, increased metabolic oxygen requirements (shivering), and coagulopathy,
I would agree with the surgeon’s suggestion, recognizing that both systemic and regional hypothermia have been shown to limit ischemic injury to the spinal cord and kidneys (Class IIa recommendation).
Therefore, since active cooling via extracorporeal circulation is not an option when utilizing a “clamp and sew” technique (no bypass), I would allow the patient to cool to 30-34ºC (passive cooling).
I would also consider utilizing regional hypothermia, which would involve the epidural infusion of 4ºC saline and/or the direct instillation of cold renal preservation fluid into the renal artery (using cold LR at 4ºC)
- Clinical Note:*
- Hypothermia decreases cerebral and spinal cord oxygen requirements by 5% for each 1 degree derease below 36ºC.
Intra-operative Management:
With application of the clamp, his blood pressure increases to 185/95 mmHg and you notice ST depression on the EKG.
What are you going to do?
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
I would:
- immediately ask the surgeon to release the cross clamp,
- ensure adequate ventilation with 100% oxygen, and
- optimize hemodynamic variables.
- If the ST depression improved with release of the cross-clamp, I would – lower the systolic blood pressure with a vasodilator such as – esmolol, SNP, NTG, or nicardipine;
- place a TEE, if not already done; and
- have the surgeon slowly reapply the clamp, while being prepared to quickly treat any subsequent pre-clamp hypertension.
My goal is to reduce the afterload enough to avoid cardiac ischemia, while at the same time maintaining adequate perfusion fo the coronaries and tissues distal to the aortic clamp.
- To this end, I would carefully administer inotropes and vasodilators while monitoring the EKG, TEE, SSEP and MEP signals, and both proximal and distal arterial lines.
Additionally, since the patient is intolerant of higher proximal pressures, I may ask the surgeon to place a temporary shunt or initiate partial bypass to improve distal perfusion and avoid ischemic injury.
Intra-operative Management:
You start a sodium nitroprusside infusion.
The medical student asks you about toxicity.
What will you tell him?
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
When sodium nitroprusside enters a red blood cell, a nonenzymatic reaction results in the release of nitric oxide and the formation of cyanide ions.
These ions can then:
- react with methemoglobin to form cyanmethemoglobin;
- react with thiosulfate to form thiocyanate; or
- bind to tissue cytochrome oxidase, which impairs normal tissue oxygen utilization.
This impaired oxygen utilization leads to cyanide toxicity, characterized by –
- metabolic acidosis,
- increased venous oxygen content,
- cardiac arrhythmias, and
- tachyphylaxis.
The risk of developing cyanide toxicity is minimal when using doses less than 0.5 mg/kg/h.
Intra-operative Management:
What are your treatment options?
(for treating toxicity from sodium nitroprusside)
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
Treating acute cyanide toxicity involves –
- discontinuing the infusion,
- mechanically ventilating the patient with 100% oxygen, and
- administering sodium thiosulfate
- (provides substrate for the 2nd reaction),
- amyl nitrate (inhaler) or sodium nitrate
- (both of which oxidize hemoglobin to methemoglobin, thereby increasing the substrate for the 1st reaction), or
- hydroxycobalamin
- (combines with cyanide ions to form cyanocobalamin, a.k.a. vitamin B12).
Administration of these drugs results in chemical reactions that effectively remove excess cyanide ions from circulation, so they are unavailable to react with tissue cytochrome oxidase.
Intra-operative Management:
What preparations would you make prior to release of the aortic cross-clamp?
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
Prior to release of the aortic cross-clamp, I would:
- decrease the depth of anesthesia (particularly volatile agents);
- administer a vasodilator (i.e., nitroglycerine or sodium nitroprusside) to facilitate volume loading;
- utilize TEE and/or a pulmonary artery catheter to guide volume loading and aid in the rapid identification and treatment of hemodynamic instability;
- discontinue any vasodilators just prior to cross-clamp release (including those utilized to assist volume loading);
- correct any electrolyte abnormalities, acid-base disturbances, or coagulopathy;
- have inotropes and vasopressors available to treat any sustained reduction in SVR following cross-clamp release; and
- ask the surgeon to release the cross-clamp gradually, allowing sufficient time for physiologic compensation and/or medical intervention.
Intra-operative Management:
After release of the aortic cross-clamp the pressure decreases to 82/40 mmHg.
Is this expected?
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
Yes.
Central hypovolemia (secondary to –
- increased venous capacitance below the clamp,
- decreased systemic vascular resistance below the clamp,
- increased capillary permeability, and
- blood loss)
- combined with lower extremity washout of vasoactive and cardiodepressant mediators can lead to – significant hypotension.
In this case, I would:
- start a fluid bolus,
- place the patient in the trendelenburg position,
- administer a vasopressor, and
- attempt to identify any other potential causes or contributing factors to hypotension, such as – hemorrhage (low filling pressures, surgical and/or anesthesiologist observation), arrhythmia, anesthetic-induced cardiovascular depression, myocardial ischemia (wall-motion abnormalities, EKG changes, elevated filling pressures), tension pneumothorax, metabolic and electrolyte abnormalities, citrate-induced hypocalcemia, and hypothermia.
- If the hypotension persisted, I would – ask the surgeon to reapply the aortic cross-clamp,
- correct any abnormalities (i.e. anemia, arrhythmia, myocardial ischemia, tension pneumothorax, and metabolic abnormalities),
- decrease the depth of anesthesia (particularly volatile agents), and
- volume load the patient (vasodilators such as nitroprusside and/or nitroglycerin may facilitate volume loading, but these should be discontinued before unclamping).
- I would then – ask the surgeon to gradually release the cross-clamp to prevent further hypotension by allowing time for physiologic compensation.
Post-operative Management:
Postoperatively, you get a call from the nurse in the ICU. She says the patient’s urine output has only been 20cc over the past 2 hours.
How would you evaluate and manage this situation?
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
Since the mortality rate for post-operative renal failure following aortic surgery is greater than 40%, I would aggressively evaluate and treat this oliguria.
First, I would examine the patient and review PA catheter data, vital signs, fluid administration, blood transfusion history, and administered medications.
Then, I would optimize the patient hemodynamically, inspect the Foley catheter for signs of obstruction, and give a fluid bolus.
If there were no apparent cause for the oliguria, I would order serum and urine electrolytes to calculate the fractional excretion of sodium, and consider a nephrology consult.
Post-operative Management:
What do you think is the cause of his renal failure?
- (A 5’6”, 175 pound, 69-year-old, male presents for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm.*
- PMH: His history includes CAD, HTN, CHF, aortic stenosis, chronic kidney disease, and 52 years of tobacco use. He leads a sedentary lifestyle and denies any history of orthopnea, PND, syncope, near-syncope, or peripheral edema. He denies ever having chest pain, but does have shortness of breath, which he attributes to smoking and lack of exercise.*
- Allergies: PCN causes a rash.*
- Medications: Atenolol, Lisinopril, HCTZ, sublingual NTG, Digoxin, ASA*
- PE: Vital Signs: BP = 140/87 mmHg; HR = 78; R = 17; T = 36.9 C*
- Airway: Mallampati class II; good neck range of motion; large tongue*
- CV: RRR*
- Pulmonary: distant breath sounds; bibasilar crackles*
- Abdomen: pulsatile abdominal mass*
- Laboratory: H/H = 13.8/51; K+ = 3.2; BUN/Cr = 31/1.9; Creatinine Clearance = 50 mL/minute.*
- ABG: pH = 7.30, PaCO2 = 44, PaO2 = 80 on room air*
- Examiner Note: BUN (normal): 5-20 mg/dL ; Creatinine (normal): Male: 0.6-1.2 mg/dL; Female: 0.5 - 1.1 mg/dL*
- CXR: flattened diaphragm bilaterally; cardiomegaly; tortuous aorta*
- ECG: NSR; LVH; Q-waves in leads II, III, and aVF*
- CT: 8 cm aneurysm extending from the supraceliac aorta to the infrarenal abdominal aorta*
- DSE: Akinesis of the inferior and lateral walls of the left ventricle (not affected by exertion)*
His renal failure is most likely the result of –
- aortic cross-clamp application and/or
- exposure to intravascular contrast dye.
Other potential causes or contributing factors include –
- potentially nephrotoxic drugs (he is taking ASA and an ACE inhibitor),
- his various comorbidities (CHF, HTN, CKD, atherosclerosis), and
- the reinfusion of unwashed salvaged blood
- (high levels of free hemoglobin – found in unwashed blood collected from chest tubes and wound drains – can be nephrotoxic when adminsitered to patients with impaired renal function).
Cross-clamp application to the aorta (even when infrarenal) is associated with –
- increased renal vascular resistance,
- decreased renal perfusion,
- decreased renal cortical blood flow, and
- acute renal failure (almost always acute tubular necrosis).
Contrast media exposure has direct cytotoxic effects on the kidneys, enhances cellular damage caused by reactive oxygen species, and increases renal vascular resistance.
In general, postoperative renal failure may be due to –
- renal ischemia,
- nephrotoxins,
- air embolization, or
- activation of the renin-angiotensin system;
Risk factors include –
- advanced age,
- prolonged cross-clamp time,
- cardiac disease, and
- preexisting renal disease.
