UBP 1.6 (Long Form): Cardiovascular - Endarterectomy Flashcards
Secondary Subject -- Coronary Artery Disease / Preoperative Cardiac Evaluation / Deep and Superficial Cervical Plexus Blocks / Neurophysiologic Monitoring / Neurophysiology / Myocardial Preconditioning / Delayed Emergence / Post-CEA Respiratory Distress / Cerebral Hyperperfusion Syndrome
Intra-Operative Management:
How would you provide regional anesthesia for this case?
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
In order to provide an effective regional anesthetic for this case, I would perform deep and superficial cervical plexus blocks to anesthetize the C2-C4 dermatomes.
The superficial cervical plexus block is performed by injecting 10 mL of local anesthetic along the posterior border of the sternocleidomastoid.
The deep cervical plexus block is performed by drawing a line from the mastoid process to Chassaignac’s tubercle at the level of the cricoid cartilage.
The C2 transverse process can then be palpated 1-2 cm caudad to the mastoid process, with the transverse processes of C3 and C4 lying at 1.5 cm intervals along the line drawn.
The block is then performed by injecting 10 cc of local anesthetic at each transverse process.
Intra-Operative Management:
What are the complications of deep and superficial cervical plexus blocks?
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
Complications of cervical plexus blockade are related mostly to the deep cervical plexus block and include:
- epidural and subarachnoid injection,
- phrenic nerve blockade,
- intravascular injection into the vertebral artery,
- recurrent laryngeal nerve blockade, and
- Horner’s syndrome (ptosis-drooping eyelid, miosis-constriction of the pupil , anhidrosis-decreased sweating, conjunctival redness, enophthalmos-ptosis gives the impression of posterior displacement of the eyeball within the orbit).
Complications associated with the superficial cervical plexus block are minimal and include:
- local anesthetic toxicity,
- bleeding, and
- infection.
Intra-Operative Management:
Do you need to perform a deep cervical plexus block to provide adequate analgesia?
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
(Online UBP – Dr. George answers it well)
CEA has been performed under superficial cervical plexus blockade alone, but in this patient with poorly controlled HTN, CAD, and CHF,
I would be concerned that a superficial cervical plexus block alone would prove inadequate (because it has a higher failure rate).
–
The sympathetic response associated with patient discomfort could lead to hypertension with its detrimental effects on the heart, requiring the administration of intravenous vasodilators, sedatives, and/or analgesics.
Providing intravenous anesthetics is problematic in that respiratory depression could lead to the loss of an unsecured airway or hypercapnia, with the latter causing redistribution of blood flow away from ischemic areas of the brain (dilation of normal cerebral vessels results in “intracerebral steal” of blood from already maximally dilated vessels in ischemic areas of the brain).
- Clinical Note:*
- An isolated superficial cervical block may be sufficient since the injected medicine often spreads to the deep cervical nerve roots.
Intra-Operative Management:
Which monitors would you place for this case?
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
- (Asked in UBP Online “pre-op” section)*
- –*
In addition to the standard ASA monitors, I would place –
an arterial line, monitor leads II and V5 of the ECG, and utilize computerized ST-segment analysis.
While the placement of a central line and PA catheter is usually not necessary, I would consider it in this case due to her significant cardiovascular disease (i.e. history of MI and 30% ejection fraction).
I would obtain central access via the subclavian, brachial, or femoral artery insertion sites to avoid accidental carotid artery puncture, which could lead to hematoma and a subsequent reduction in cerebral perfusion.
If general anesthesia were planned, I would consider TEE (instead of central venous or pulmonary artery catheterization) and intra-operative neurologic monitoring for cerebral ischemia (i.e. EEG, SSEPs, transcranial Doppler, stump pressure, and cerebral oximetry).
Xtra Q – Where would you place your Central Line?
Intra-Operative Management:
You are just finishing placing a central venous line and a pulmonary artery catheter, when the resident asks you what options are available for neurologic monitoring.
What would you say?
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
(Asked in UBP Online “Pre-op” section)
The most reliable monitor of neurologic function is the –
inter-operative exam of the awake patient,
which should include an assessment of the patient’s level of consciousness, speech, and contralateral handgrip.
–
However, for patients undergoing general anesthesia, indirect monitoring of cerebral perfusion must be employed to identify cerebral ischemia and those who require shunting.
There are a variety of indirect neurologic monitoring techniques available, including –
- stump pressure determinations,
- EEG,
- SSEPs,
- transcranial Doppler,
- cerebral oximetry,
- measurement of regional cerebral blood flow, and
- jugular venous oxygen saturation measurements.
- UBP Online Note = If your surgeon routinely shunts, you may NOT need neuromonitoring.*
- —-*
- Clinical Notes:*
-
Stump pressure (internal carotid artery):
- The stump pressure is obtained by placing a needle in the artery above the clamp to measure the back pressure resulting from collateral flow through the circle of Willis.
-
Advantages:
- inexpensive,
- easy to obtain,
- continuously available during cross-clamping
- The measurement of stump pressure is questionably beneficial in selecting patients for carotid shunting
- The critical stump pressure is unknown, but pressures < 50 mmHg are associated with hypoperfusion
-
Regional cerebral blood flow measurements (rCBF)
- Regional cerebral blood flow measurements are obtained by intravenous or ipsilateral carotid artery injection of radioactive xenon, with subsequent analysis.
- Few centers utilize this modality due to the expense and expertise required.
-
EEG monitoring
- A stable anesthetic is required when utilizing this modality.
-
Disadvantages:
- may NOT detect subcortical or small cortical infarcts,
- false-negatives are not uncommon (especially for those with preexisting neurologic deficits), and
- not specific for ischemia (false positives), since the EEG may be altered with changes in temperature, blood pressure, and anesthetic depth.
-
SSEP monitoring
- SSEP monitoring measures the response of the sensory cortex to electrical impulses from peripheral sensory nerve stimulation (the sensory cortex is primarily supplied by the middle cerebral artery).
- No specific reduction in amplitude or increase in latency has been established as a marker for cerebral ischemia.
- SSEP readings are affected by hypothermia, blood pressure, anesthetic depth, leading to false positives (false negatives also occur).
-
Transcranial Doppler ultrasonography (TCD)
- TCD of the ipsilateral middle cerebral artery allows for the continuous measurement of mean blood flow velocity and the detection of micro-embolic events.
- TCD may be helpful in evaluating shunt function, identifying shunt malfunction and embolization during shunt insertion, determining the need for shunt placement (if there is decreased flow during cross-clamp application), and in managing postoperative hyper-perfusion.
-
Cerebral Oxygenation
- Jugular bulb venous oxygen saturation monitoring allows for the determination of the arterial-venous oxygen content difference and jugular venous oxygenation → these measurements provide information on global cerebral oxygen saturation.
-
Cerebral oximetry –
- monitors regional cerebral oxygen saturation through the scalp and skull.
- Cerebral oximetry measures the oxygen saturation in the entire tissue bed (brain tissue, arterial blood, and venous blood).
- The measurement approximates venous blood saturation since the tissue bed consists primarily of venous blood.
- Transconjunctival oxygen tension
- A relative decrease of 20% or greater in regional cerebral oxygen saturation is suggestive of cerebral ischemia
Intra-Operative Management:
The patient refuses regional anesthesia.
Would you monitor neurological function intra-operatively?
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
If the surgeon utilized selective carotid artery shunting,
I would employ some form of neurological monitoring to aid in determining whether this patient required shunt placement.
Secondarily, neurological monitoring may help to identify patients who would benefit from blood pressure augmentation.
While the available evidence does not adequately demonstrate improved outcomes, neurologic monitoring may– reduce the need for shunt placement, warn of improper shunt placement, and prevent unnecessary augmentation of blood pressure with its detrimental effects on the heart.
However, none of the currently available monitoring techniques is completely reliable and without limitations.
Intra-Operative Management:
How would you induce general anesthesia?
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
- *Listen to how Dr. George answers this online**
- *Could answer by – my goals are… Therefore, I would…*
In an effort to maintain adequate cerebral perfusion and minimize stress to the heart, I would:
- avoid any hypercarbia or hypoxia,
- prepare to treat any hypertension, tachycardia, bradycardia, or hypotension that develops during induction with short acting agents (i.e. phenylephrine, esmolol, nitroglycerine, and sodium nitroprusside),
- place the appropriate monitors and lines,
- pre-oxygenate the patient,
- start a remifentanil drip and administer esmolol and lidocaine to blunt the sympathetic response to laryngoscopy, and
- slowly titrate etomidate until the patient was no longer responsive (propofol and etomidate reduce the cerebral metabolic rate proportionately more than cerebral blood flow). After I had proven the ability to mask ventilate, I would –
- administer a muscle relaxant (keep in mind that succinylcholine should be avoided in hemiparetic patients),
- ventilate the patient with a volatile agent, and
- perform laryngoscopy after achieving a sufficient depth of anesthesia.
–
The use of a short acting narcotic would avoid the post-operative sedation and respiratory depression that could delay early neurologic assessment.
Utilizing etomidate would provide superior hemodynamic stability in this patient with chronic hypertension, likely hypovolemia, and significant cardiac disease.
Intra-Operative Management:
Would ketamine be acceptable?
(for induction of general anesthesia?)
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
Why/Why Not?
While small doses would probably be acceptable,
ketamine would not be my first choice in this patient with coronary artery disease.
The sympathomimetic effects of ketamine could result in increased systemic vascular resistance, heart rate, and cardiac output with subsequent detrimental increases in myocardial oxygen demand.
Therefore, I believe etomidate would be the better choice for induction.
Intra-Operative Management:
How would you maintain anesthesia?
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
Is Isoflurane the best volatile anesthetic for this case?
I would maintain anesthesia with a remifentanil infusion and low dose Sevoflurane (0.5 MAC) to allow EEG monitoring and maintenance of blood pressures in the high-normal range during cross-clamp application (collateral perfusion is driven by systolic blood pressure).
–
While Isoflurane produces a decrease in cerebral metabolic rate up to 50% when the EEG is isoelectric, the dose required to produce an isoelectric EEG would cause significant cardiac depression and interfere with EEG monitoring of cerebral perfusion.
The newer volatile agents, Sevoflurane and Desflurane, also cause a dose dependent decrease in cerebral metabolic rate, and have the advantage of allowing rapid emergence from anesthesia for early neurologic assessment in the operating room.
Intra-Operative Management:
What is myocardial preconditioning?
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
Pharmacologic preconditioning is when exposure to certain drugs serves to protect the myocardium against subsequent myocardial ischemia and reperfusion injury.
Volatile agents at concentrations as low as 0.25 MAC may limit infarct size, prevent dysrhythmias, and preserve myocardial function.
The mechanism is not well defined but involves the opening of mitochondrial K+-ATP channels, which prevent mitochondrial calcium overload.
Pharmacologic preconditioning has been demonstrated with Isoflurane, Sevoflurane, and Desflurane with similar efficacy.
Given this patient’s significant CAD, she may benefit from pharmacologic preconditioning should cardiac ischemia occur.
Intra-Operative Management:
A few minutes into the case, you note the patients end-tidal CO2 is above her preoperative baseline.
Does this concern you?
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
Assuming this were an acute change rather than a chronic condition resulting from preexisting pulmonary disease (secondary to 40 years of tobacco abuse), I would be concerned.
An acute increase in PaCO2 can lead to cerebral vasodilation in normally reactive, non-ischemic, vascular beds, thus diverting blood flow away from hypoperfused areas of the brain where the vasculature is already maximally dilated (“steal” phenomenon).
On the other hand, significant hypocarbia can exacerbate cerebral ischemia secondary to intense vasoconstriction and leftward shifting of the oxyhemoglobin dissociation curve (the latter results in impaired oxygen delivery to tissues).
Therefore, the maintenance of normocarbia is recommended during CEA.
Clinical Notes:
- Cerebral vasoconstriction associated with hypocarbia could theoretically lead to the diversion of blood from normally perfused areas of the brain to hypoperfused areas. However, animal studies have demonstrated that significant hypocarbia exacerbates ischemia.
- In hypoperfused areas of the brain, cerebral vessels dilate in order to improve perfusion. Over time these vessels begin to exhibit a blunted response to changes in carbon dioxide.
—
Xtra Q – What is the difference between carotid body and carotid sinus?
Intra-Operative Management:
During dissection, the patient’s heart rate drops to 48 beats per minute and her blood pressure falls to 88/40 mmHg.
What is your differential diagnosis?
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
The most likely cause of this change in vital signs is –
reflex bradycardia secondary to enhanced vagal tone from surgical manipulation of the carotid sinus with activation of carotid baroreceptors.
However, this hypotension and bradycardia could also be the result of – myocardial depression, ischemia, or dysrhythmia.
Finally, any preexisting autonomic neuropathy and/or the previous administration of B-blockers and/or vasodilators could be contributing to her hypotension.
Intra-Operative Management:
During dissection, the patient’s heart rate drops to 48 beats per minute and her blood pressure falls to 88/40 mmHg.
What would you do?
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
I would –
- ask the surgeon to stop any further dissection;
- quickly evaluate the ECG tracing, PA pressures, and cardiac output; and
- make sure the patient was adequately ventilated and oxygenated.
Depending on the etiology, I would – treat with atropine, fluids, and/or inotropic agents.
If I felt the etiology were manipulation of the carotid baroreceptors, I would – ask the surgeon to infiltrate the area with local anesthetic with the goal of preventing further episodes to reflex bradycardia.
However, infiltration at the carotid bifurcation may also result in increased post-operative hypertension (secondary to blunting of the normal baroreceptor response to hypertension).
- Clinical Note:*
- The normal baroreceptor response to elevations in blood pressure is to increase baroreceptor discharge, with subsequently enhanced vagal tone and inhibited systemic vasoconstriction.
Intra-Operative Management:
Shortly after placement of the carotid cross clamp, ipsilateral EEG slowing is noted.
What is the significance of this change in the EEG?
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
Reduced wave frequency and attenuation of wave amplitude may indicate cerebral ischemia;
if the ischemia becomes severe the EEG tracing may become completely isoelectric.
While hypothermia and increased depth of anesthesia can produce similar EEG changes, these changes are usually bilateral as opposed to the unilateral EEG changes associated with hemispheric ischemia.
In this patient’s case, the reduced EEG frequency is one sided and, therefore, more suggestive of hemispheric ischemia.
Xtra Q: What would you do?
In response to these changes, I would ask the surgeon to remove the cross clamp and consider placing a shunt to restore cerebral blood flow.
In addition, I would ventilate with 100% FiO2, ensure adequate MAP, ensure normocapnea, and consider pharmacologic brain protection as hemodynamically tolerated.
Intra-Operative Management:
Despite these interventions, the EEG tracing continues to show ipsilateral slowing and the surgeon wants you to raise the SBP to 180 mmHg.
Would you agree to do this?
- (A 68-year-old, 72 kg woman presents to the operating room for urgent left carotid endarterectomy. She has experienced multiple unilateral transient ischemic attacks over the past week.*
- Meds: Digoxin, furosemide, nifedipine, aspirin, NTG prn*
- Allergies: NKDA*
- PMH: Her past medical history includes poorly controlled HTN, IDDM, 40 years of tobacco use, and an MI that occurred one year ago with subsequent moderate CHF. She underwent cardiac catheterization eight months ago with PCA to the RCA. Her ejection fraction is 30%, and she experiences occasional exertional angina and orthopnea*
- PE: Vital signs: P = 68, BP = 155/83 mmHg, RR = 22, T = 37 °C*
- Airway: Mallampati II, Thyromental Distance > 3 finger breadths, Edentulous*
- Neck: Left carotid bruit*
- Lungs: Rales heard in both lung bases*
- CXR: Prominent vascular markings and cardiomegaly*
- EKG: NSR, LVH, Q-waves V1-V4, nonspecific ST changes*
- Lab: Hgb = 11.5 gm/dL, Na+ = 134 mEq/L, K+ = 3.1 mEq/L)*
If I believed that her preoperative blood pressure of 170/95 mmHg was close to her baseline blood pressure (best determined by referring to multiple blood pressure readings taken during recent hospital visits, the preoperative visit, and upon admission),
I would cautiously raise her blood pressure while monitoring the ECG and CVP in an attempt to improve cerebral perfusion.
However, I recognize that raising her blood pressure could result in myocardial ischemia secondary to the increased myocardial oxygen consumption associated with increased afterload.
Therefore, I would limit any increase in systolic blood pressure to 10-15% above baseline and, if she developed any signs of myocardial ischemia, lower it to baseline, allowing some EEG slowing in exchange for adequate cardiac oxygenation.
