UBP 2.8 (Short Form): Cardiovascular – CABG Flashcards
Secondary Subject -- Perioperative β-blockade/Cardiac Enzymes/ Myocardial Ischemia/PVCs on EKG/ Cardiac Pacing/Heparin Reversal/Post-bypass Coagulopathy/Intra-operative Awareness
Would you discontinue this patient’s B-blocker preoperatively?
(A 64-year-old, 100 kg, man is brought to the operating room for CABG. He was asymptomatic until 4 days ago when he developed severe chest pain with exertion that responded to nitroglycerin (NTG) and metoprolol. Laboratory testing, at the time, was negative for the CK-MB isoenzyme, but showed elevated Troponin enzymes. His EKG showed anterolateral ST-segment depression. He has a history of congestive heart failure, poorly controlled type II diabetes mellitus, HTN, and tobacco use of 1 pack per day for the past 34 years. He has two peripheral IVs and NTG and heparin infusions running. His medications include metoprolol, NPH insulin, Digoxin, Albuterol, and Atrovent. Vital signs: P = 90, BP = 128/72 mmHg, RR = 16, T = 37.2 ºC)
Since the discontinuation of B-blocker therapy may lead to increased morbidity and mortality, I would continue his metoprolol perioperatively, if possible.
However, if a patient were not already receiving a B-blocker, I would NOT attempt to acutely establish adequate B-blockade the day of surgery
(the 2014 ACC/AHA guidelines recommendation is that the initiation of B-blocker therapy should occur at least 2-7 days prior to surgery),
recognizing that this is associated with an increased risk of bradycardia, hypotension, stroke, and total mortality (although cardiovascular morbidity and mortality is reduced).
What is the significance of a negative CK-MB, but positive Troponin enzymes?
(A 64-year-old, 100 kg, man is brought to the operating room for CABG. He was asymptomatic until 4 days ago when he developed severe chest pain with exertion that responded to nitroglycerin (NTG) and metoprolol. Laboratory testing, at the time, was negative for the CK-MB isoenzyme, but showed elevated Troponin enzymes. His EKG showed anterolateral ST-segment depression. He has a history of congestive heart failure, poorly controlled type II diabetes mellitus, HTN, and tobacco use of 1 pack per day for the past 34 years. He has two peripheral IVs and NTG and heparin infusions running. His medications include metoprolol, NPH insulin, Digoxin, Albuterol, and Atrovent. Vital signs: P = 90, BP = 128/72 mmHg, RR = 16, T = 37.2 ºC)
CK-MB, an isoenzyme of creatine kinase, is found in other tissues of the body and is less sensitive and specific for myocardial cell damage than Troponin enzymes.
The CK-MB isoenzyme is usually elevated within 4-6 hours after the onset of an acute MI, peaks in 12-24 hours and returns to baseline within 2-3 days.
Cardiac troponin serum levels, on the other hand, are usually elevated within 2-6 hours after the onset of an acute MI, peak at 12-24 hours, and may stay elevated for 7-10 days.
The fact that troponin assays are positive and CK-MB isoenzymes are negative suggests that the acute MI occurred over 2-3 days ago and that the patient has not suffered a recurrent MI in the interval.
What is the significance of ST-segment depression on the EKG?
(A 64-year-old, 100 kg, man is brought to the operating room for CABG. He was asymptomatic until 4 days ago when he developed severe chest pain with exertion that responded to nitroglycerin (NTG) and metoprolol. Laboratory testing, at the time, was negative for the CK-MB isoenzyme, but showed elevated Troponin enzymes. His EKG showed anterolateral ST-segment depression. He has a history of congestive heart failure, poorly controlled type II diabetes mellitus, HTN, and tobacco use of 1 pack per day for the past 34 years. He has two peripheral IVs and NTG and heparin infusions running. His medications include metoprolol, NPH insulin, Digoxin, Albuterol, and Atrovent. Vital signs: P = 90, BP = 128/72 mmHg, RR = 16, T = 37.2 ºC)
ST-segment depression is consistent with –
- a non-ST-elevation myocardial infarction (NSTEMI, non-Q wave myocardial infarction),
- non-infarction subendocardial ischemia (i.e. unstable angina),
- digoxin use (usually with short QT and prominent U-waves), or
- hypokalemia (usually long QT and prominent U-waves).
This patient’s elevated cardiac biomarkers (i.e. CK-MB, cardiac troponin), however, suggest that his ST-segment depression is secondary to an acute myocardial infarction.
In any case, down-sloping and/or horizontal ST depression is more specific for myocardial ischemia than is up-sloping depression.
- Clinical Note:*
- Significant ST-segment depression in two or more contiguous leads, with or without concomitant deep symmetrical T-wave inversion, is highly suggestive of unstable angina or NSTEMI. The presence of elevated cardiac biomarkers establishes the diagnosis of NSTEMI.
What are some contributing factors to myocardial ischemia?
(A 64-year-old, 100 kg, man is brought to the operating room for CABG. He was asymptomatic until 4 days ago when he developed severe chest pain with exertion that responded to nitroglycerin (NTG) and metoprolol. Laboratory testing, at the time, was negative for the CK-MB isoenzyme, but showed elevated Troponin enzymes. His EKG showed anterolateral ST-segment depression. He has a history of congestive heart failure, poorly controlled type II diabetes mellitus, HTN, and tobacco use of 1 pack per day for the past 34 years. He has two peripheral IVs and NTG and heparin infusions running. His medications include metoprolol, NPH insulin, Digoxin, Albuterol, and Atrovent. Vital signs: P = 90, BP = 128/72 mmHg, RR = 16, T = 37.2 ºC)
Myocardial ischemia occurs when there is inadequate oxygen supply to meet metabolic demands.
Causes of decreased supply include – tachycardia, anemia, hypoxia, and decreased coronary perfusion pressure (hypotension, coronary vasospasm, coronary obstruction, severe aortic stenosis, severe aortic regurgitation, and elevated left end-diastolic pressure).
Causes of increased demand include – tachycardia, increased wall tension, contractility, and increased afterload (severe hypertension).
Because the left ventricular intracavitary pressures during systole are equal to systemic pressures, LV coronary perfusion primarily occurs during diastole.
Coronary perfusion pressure equals aortic diastolic blood pressure minus the left ventricular end diastolic pressure (CPP = AoDBP - LVEDP).
Because the myocardium can only minimally increase oxygen extraction during times of increased demand, it must increase oxygen delivery by increasing coronary blood flow to avoid ischemia.
What is coronary perfusion pressure?
(A 64-year-old, 100 kg, man is brought to the operating room for CABG. He was asymptomatic until 4 days ago when he developed severe chest pain with exertion that responded to nitroglycerin (NTG) and metoprolol. Laboratory testing, at the time, was negative for the CK-MB isoenzyme, but showed elevated Troponin enzymes. His EKG showed anterolateral ST-segment depression. He has a history of congestive heart failure, poorly controlled type II diabetes mellitus, HTN, and tobacco use of 1 pack per day for the past 34 years. He has two peripheral IVs and NTG and heparin infusions running. His medications include metoprolol, NPH insulin, Digoxin, Albuterol, and Atrovent. Vital signs: P = 90, BP = 128/72 mmHg, RR = 16, T = 37.2 ºC)
Because the left ventricular intracavitary pressures during systole are equal to systemic pressures, LV coronary perfusion primarily occurs during diastole.
Coronary perfusion pressure equals aortic diastolic blood pressure minus the left ventricular end diastolic pressure (CPP = AoDBP - LVEDP).
Because the myocardium can only minimally increase oxygen extraction during times of increased demand, it must increase oxygen delivery by increasing coronary blood flow to avoid ischemia.
Physical examination reveals wheezes and decreased breath sounds in the left lower lobe. Would you require further evaluation? What tests would you order? How will that change your management? Consider the stability of the patient for further eval – such as PFTs.
(A 64-year-old, 100 kg, man is brought to the operating room for CABG. He was asymptomatic until 4 days ago when he developed severe chest pain with exertion that responded to nitroglycerin (NTG) and metoprolol. Laboratory testing, at the time, was negative for the CK-MB isoenzyme, but showed elevated Troponin enzymes. His EKG showed anterolateral ST-segment depression. He has a history of congestive heart failure, poorly controlled type II diabetes mellitus, HTN, and tobacco use of 1 pack per day for the past 34 years. He has two peripheral IVs and NTG and heparin infusions running. His medications include metoprolol, NPH insulin, Digoxin, Albuterol, and Atrovent. Vital signs: P = 90, BP = 128/72 mmHg, RR = 16, T = 37.2 ºC)
Yes.
Depending on the patient’s stability, his wheezing and decreased breath sounds would warrant further evaluation such as – a CXR, PFTs (including the response to bronchodilator therapy), echocardiography, and an ABG.
Considering his recent myocardial event and smoking history, these physical findings may represent cardiac and/or pulmonary dysfunction that requires further medical optimization prior to surgery.
Depending on the results of these studies, I may administer bronchodilators, antibiotics, or diuretics.
Additionally, a more clear understanding of the patient’s cardiopulmonary disease would aid in appropriate ventilator management and postoperative planning for extubation.
CXR shows left lower lobe atelectasis. Would you delay the case?
(A 64-year-old, 100 kg, man is brought to the operating room for CABG. He was asymptomatic until 4 days ago when he developed severe chest pain with exertion that responded to nitroglycerin (NTG) and metoprolol. Laboratory testing, at the time, was negative for the CK-MB isoenzyme, but showed elevated Troponin enzymes. His EKG showed anterolateral ST-segment depression. He has a history of congestive heart failure, poorly controlled type II diabetes mellitus, HTN, and tobacco use of 1 pack per day for the past 34 years. He has two peripheral IVs and NTG and heparin infusions running. His medications include metoprolol, NPH insulin, Digoxin, Albuterol, and Atrovent. Vital signs: P = 90, BP = 128/72 mmHg, RR = 16, T = 37.2 ºC)
Not necessarily.
This atelectasis most likely represents mucous plugging due to COPD and/or smoking.
If it were mild to moderate and not significantly interfering with oxygenation or ventilation I would proceed with the case.
If the atelectasis were severe and amenable to treatment, the patient may benefit from a short delay of surgery to allow for further treatment.
The surgeon declares the case emergent. What are your options to optimize his pulmonary status prior to this urgent operation?
(A 64-year-old, 100 kg, man is brought to the operating room for CABG. He was asymptomatic until 4 days ago when he developed severe chest pain with exertion that responded to nitroglycerin (NTG) and metoprolol. Laboratory testing, at the time, was negative for the CK-MB isoenzyme, but showed elevated Troponin enzymes. His EKG showed anterolateral ST-segment depression. He has a history of congestive heart failure, poorly controlled type II diabetes mellitus, HTN, and tobacco use of 1 pack per day for the past 34 years. He has two peripheral IVs and NTG and heparin infusions running. His medications include metoprolol, NPH insulin, Digoxin, Albuterol, and Atrovent. Vital signs: P = 90, BP = 128/72 mmHg, RR = 16, T = 37.2 ºC)
My options would include –
bronchodilator therapy, chest physiotherapy, incentive spirometry, and post-intubation alveolar recruitment maneuvers.
If there was evidence of cardiogenic pulmonary edema, I would consider diuretics.
His digoxin level is 2.2 ng/mL. What do you think about this level?
(A 64-year-old, 100 kg, man is brought to the operating room for CABG. He was asymptomatic until 4 days ago when he developed severe chest pain with exertion that responded to nitroglycerin (NTG) and metoprolol. Laboratory testing, at the time, was negative for the CK-MB isoenzyme, but showed elevated Troponin enzymes. His EKG showed anterolateral ST-segment depression. He has a history of congestive heart failure, poorly controlled type II diabetes mellitus, HTN, and tobacco use of 1 pack per day for the past 34 years. He has two peripheral IVs and NTG and heparin infusions running. His medications include metoprolol, NPH insulin, Digoxin, Albuterol, and Atrovent. Vital signs: P = 90, BP = 128/72 mmHg, RR = 16, T = 37.2 ºC)
Therapeutic levels of digoxin are 0.5-2.0 ng/mL.
Digoxin toxicity may result in EKG changes, arrhythmias, fatigue, hypersalivation, confusion, nausea and vomiting, and visual disturbances.
Moreover, even in the therapeutic range, digoxin may lead to mild ST depression in multiple ECG leads, potentially compromising my ability to monitor for cardiac ischemia using this modality.
Finally, the acid-base and electrolyte abnormalities that often occur following cardiopulmonary bypass may exacerbate his toxicity.
Therefore, if not already done, I would talk to the cardiologist about discontinuing the drug until after surgery.
Additionally, I would be careful to avoid any factors that would potentiate toxicity, such as – hypokalemia, hypomagnesemia, and hypercalcemia.
