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3 Preoperative Evaluation andRisk Assessment

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Table 3.1

Medication class Perioperative management Rationale

ACE inhibitors, ARBs

Steroids Continue to the day of surgery; if >10mg/

Diabetes medications

Insulin Continue normal regimen with the

Metformin Hold 2days prior to OR • Prevent hypoglycemia and

GLP-1 inhibitors Hold at least 24h prior to surgery • Prevent hypoglycemia SGLT2

DVT prophylaxis Heparin 5000units SC Q8 h or Lovenox

Anti-arrhythmics Continue through day of surgery

NSAIDs Stop 7days prior to surgery

(continued)

inhibitors (Canagliozin, dapagliozin, empagliozin)

Stop 2days prior to surgery

day and taking for at least 1week, will need stress dose steroids intra-op+postoperative taper

evening meal the night before surgery Hold the morning of surgery (Note—may additionally depend on whether rst or second case)

Stop 7days prior to surgery

40mg SC Q24 h should be ordered on all preoperative patients at the time of consultation unless they are on any form of IV anticoagulation or there is a contraindication. Last dose of SC heparin should be given evening before surgery. Lovenox, last dose given morning prior to surgery

Amiodarone—consider TSH, PFTs if planning to continue for extended period postoperatively

• Decrease risk for intra-op and postop vasoplegia and kidney injury

• Patient may have adrenal suppression secondary to high-dose and/or chronic steroid usage and be unable to mount an endogenous, physiologic stress response

• Avoid hypoglycemia

avoid increased risk of metabolic acidosis

• Avoid potential risk of ketoacidosis

• Mitigate thrombotic risk in patients with cardiovascular pathology

• Maintain normal rhythm for hemodynamic stability; minimize cardiac metabolic stress

• Amiodarone can adversely affect the thyroid and lungs, so a baseline assessment will help with monitoring if drug is used long term

• Reversible inhibitors of platelet aggregation; recovery of platelet function in hours to days (based on agent half-life)

(continued)

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E. A. Calle and D. M. Shahian

Table 3.1

Medication class Perioperative management Rationale

Beta-blockers Continue regular dose day of surgery

Vitamins and supplements, including sh oil, omega-3 fatty acids, ginger, garlic, ginkgo

Glaucoma drops Check with anesthesiologist

ASA acetylsalicylic acid (aspirin), ACE angiotensin converting enzyme, Ab atrial brillation, AVR aortic valve replacement, DES drug-eluting stent, DOAC direct oral anticoagulant, GLP-1 glucagon- like peptide-1, IABP intra-aortic balloon pump, IV intravenous, MR mitral regurgitation, MVR mitral valve replacement, OR operating room, PFTs pulmonary function tests, SC subcutaneous, TSH thyroid function studies, VAD ventricular assist device

Bridge: replacing home anticoagulant with IV heparin since heparin has a shorter half-life than all of the oral anticoagulants. This allows the patient to remain on therapeutic anticoagulation as close to surgery as possible, to minimize the risk of thrombosis

(continued)

Consider changing regimen from long-acting home agent to fractionated, short-acting agents—e.g., convert long-acting metoprolol succinate (Toprol-XL) to metoprolol tartrate (Lopressor)

Discontinue all at least 7days prior to surgery

Generally best to administer day of surgery

• Abrupt withdrawal (unless necessary for hypotension or bradycardia) may lead to rebound tachycardia, hypertension, or ischemia

• Change to short acting allows tighter control and more exibility if blood pressure has greater uctuation in immediate peri-op and postoperative period

• Some may interfere with platelet function [1]

• Avoid interactions with perioperative medications such as anxiolytics, sedatives, anesthetics, analgesics, and postoperative medications, including anticoagulants

• Prevent excessive elevation

of intra-ocular pressure during prolonged cardiopulmonary bypass and potential ischemic neuropathy

Acknowledgments

team members of Massachusetts General Hospital Cardiac Surgery, for discussion and collation of local practice guidelines.

Thank you to Alysia Monaco, N.P., Chis Stager, P.A., and all the staff and

References

1. Bojar RM.Manual of perioperative care in adult cardiac surgery. 6th ed. Hoboken: Wiley; 2021.

2. Lilly LS, editor. Pathophysiology of heart disease: an introduction to cardiovascular medicine. 7th ed. Alphen aan den Rijn: Wolters Kluwer; 2021.

3. Ruff CT, O’Gara PT.Preoperative evaluation for cardiac surgery | Cardiac surgery in the adult, 5th ed. | AccessSurgery | McGraw Hill Medical. https://accesssurgery.mhmedical.com/content.

aspx?bookid=2157§ionid=164288767. Accessed 31 May 2022.

3 Preoperative Evaluation andRisk Assessment

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4. Araujo L, Dombrovskiy V, Kamran W, Lemaire A, Chiricolo A, Lee LY, Lemaire A. The effect of preoperative liver dysfunction on cardiac surgery outcomes. J Cardiothorac Surg. 2017;12:73. https://doi.org/10.1186/s13019- 017- 0636- y.

5. Jacob KA, Hjortnaes J, Kranenburg G, de Heer F, Kluin J.Mortality after cardiac surgery in patients with liver cirrhosis classied by the Child-Pugh score. Interact Cardiovasc Thorac Surg. 2015;20:520–30.

6. Modi A, Vohra HA, Barlow CW.Do patients with liver cirrhosis undergoing cardiac surgery have acceptable outcomes? Interact Cardiovasc Thorac Surg. 2010;11:630–4.

7. Morimoto N, Okada K, Okita Y.The model for end-stage liver disease (MELD) predicts early and late outcomes of cardiovascular operations in patients with liver cirrhosis. Ann Thorac Surg. 2013;96:1672–8.

8. Gopaldas RR, Chu D, Cornwell LD, Dao TK, Lemaire SA, Coselli JS, Bakaeen FG.Cirrhosis as a moderator of outcomes in coronary artery bypass grafting and off-pump coronary artery bypass operations: a 12-year population-based study. Ann Thorac Surg. 2013;96:1310–5.

9. Cury RC, Abbara S, Achenbach S, etal. Coronary artery disease—reporting and data system (CAD-RADS): an expert consensus document of SCCT, ACR and NASCI: endorsed by the ACC.JACC Cardiovasc Imaging. 2016;9:1099–113.

10. Ipek EG, Blumenthal R, Sharma G.Non-invasive assessment of myocardial viability. In: Latest in cardiology; 2020. https://www.acc.org/latest- in- cardiology/articles/2020/08/14/07/44/

non- invasive- assessment- of- myocardial- viability.

11. Garcia MJ, Kwong RY, Scherrer-Crosbie M, Taub CC, Blankstein R, Lima J, Bonow RO, Eshtehardi P, Bois JP.State of the art: imaging for myocardial viability: a scientic statement from the American Heart Association. Circ Cardiovasc Imaging. 2020;13:e000053. https://doi.

org/10.1161/HCI.0000000000000053.

12. Albouaini K, Egred M, Alahmar A, Wright DJ.Cardiopulmonary exercise testing and its application. Postgrad Med J. 2007;83:675–82.

13. Li Y, Walicki D, Mathiesen C, Jenny D, Li Q, Isayev Y, Reed Iii JF, Castaldo JE.Strokes after cardiac surgery and relationship to carotid stenosis. Arch Neurol. 2009;66(9):1091–6.

14. Naylor AR, Ricco JB, de Borst GJ, etal. Editor’s choice—management of atherosclerotic carotid and vertebral artery disease: 2017 clinical practice guidelines of the European Society for Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg. 2018;55:3–81.

15. Santarpino G, Nicolini F, de Feo M, etal. Prognostic impact of asymptomatic carotid artery stenosis in patients undergoing coronary artery bypass grafting. Eur J Vasc Endovasc Surg. 2018;56:741–8.

16. Sultan I, Bianco V, Kilic A, etal. Predictors and outcomes of ischemic stroke after cardiac surgery. Ann Thorac Surg. 2020;110:448–56.

17. Klarin D, Patel VI, Zhang S, etal. Concomitant carotid endarterectomy and cardiac surgery does not decrease postoperative stroke rates. J Vasc Surg. 2020;72:589–596.e3.

18. Giri J, Nathan A.How should we address carotid artery stenosis around the time of open-heart surgery? JACC Cardiovasc Interv. 2017;10(3):299–301.

19. AbuRahma AF, Avgerinos ED, Chang RW, et al. Society for Vascular Surgery clinical practice guidelines for management of extracranial cerebrovascular disease. J Vasc Surg. 2022;75:4S–22S.

20. Shahian DM, Jacobs JP, Badhwar V, etal. The Society of Thoracic Surgeons 2018 adult cardiac surgery risk models: part 1—background, design considerations, and model development. Ann Thorac Surg. 2018;105:1411–8.

21. Hornor MA, Duane TM, Ehlers AP, Jensen EH, Brown PS, Pohl D, da Costa PM, Ko CY, Laronga C.American College of Surgeons’ guidelines for the perioperative management of antithrombotic medication. J Am Coll Surg. 2018;227:521–536.e1.

Chapter 4

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Echocardiography

JordanSecor andEvinYucel

Transthoracic Echocardiography (TTE)

• Non-invasive, performed with handheld probe on chest surface

• Allows evaluation of the structure and function of the atria, ventricles, valves,

great vessels, and pericardium

• Ultrasound (US) probe emits US wave and detects US waves as they are reected

through patient’s tissue, air, and uid within body back to the probe

• US machine software creates images and measurements using the detected US

waves based on the known frequency and intensity of the energy emitted by the probe

• Doppler echocardiography displays blood ow in cardiac chambers and vessels

based on the change in frequency imparted to a sound wave by the movement of erythrocytes and is used to quantify hemodynamic effects of valve lesions and intracardiac shunts

• Pulsed Doppler and continuous wave Doppler can be utilized to measure pres-

sure gradient change in between two cardiac chambers. Color Doppler permits the assessment of the presence and direction of blood ow

• Performed at the bedside without sedation

• Anesthesiologists, intensive care physicians, surgeons, and cardiologists per-

form TTE at bedside and in operating room (OR)

• Provides real-time information; much faster to perform, more accessible, less

expensive, and lower risk than CT, MRI, or conventional angiography

• Limited by the knowledge and experience of the providers capturing and inter-

preting the images

J. Secor · E. Yucel (*) Massachusetts General Hospital, Boston, MA, USA e-mail: jsecor@mgb.org; eyucel@mgh.harvard.edu

Switzerland AG 2024 J. P. Bloom, T. M. Sundt (eds.), Cardiac Surgery Clerkship, Contemporary Surgical Clerkships, https://doi.org/10.1007/978-3-031-41301-8_4

49© The Author(s), under exclusive license to Springer Nature

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Fig. 4.1 Transthoracic echocardiography views. (a) Parasternal long axis view showing left ven- tricle (LV), left atria (LA), mitral valve (MV), aortic valve (AOV), aorta (Ao) and right ventricle (RV). (b) Parasternal short axis view showing aortic valve (AOV) and interatrial septum (IAS). (c) Apical 4 chamber view showing both ventricles (RV and LV), both atria (LA and RA) along with tricuspid valve (TV) and mitral valve (MV). (d) Subcostal view showing all chambers of the heart and the inferior aspect of the right ventricle with liver in view

J. Secor and E. Yucel

• “Formal” TTE studies performed by ultrasound technicians are interpreted by

cardiologists

• Standard TTE windows are parasternal, apical, subcostal, and suprasternal

(Fig.4.1)

• Cardiac surgeons must be familiar with the applications, interpretation, and limi-

tations of TTE

Transesophageal Echocardiography (TEE)

• Ultrasound probe is placed into the esophagus to visualize structures in more

detail and requires sedation

• Similar to TTE, TEE relies on the emission and detection of US waves

4 Echocardiography

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• Requires specialized training, typically only cardiac anesthesiologists and cardi-

ologists perform TEE

• Carries roughly ~1in 10,000 risk of esophageal perforation

• Signicantly better than TTE at visualizing posterior structures (left atrium, left

ventricle, mitral valve, descending aorta) and prosthetic valves

• Performed in the OR before, during, and after many cardiac surgery operations

• Can be used to make decisions regarding the adequacy of an operation and evalu-

ating possible complications. Examples include evaluating for aortic dissection after cannulation of aorta for cardiopulmonary bypass, determining the extent of air in the pulmonary veins and left ventricle prior to separating from cardiopulmonary bypass, and determining presence or absence of paravalvular leak after valve replacement.

• Acoustic windows include esophageal, deep esophageal, and transgastric

(Fig.4.2)

cde

Fig. 4.2 Transesophageal echocardiography views. (a) Mid-esophageal 4-chamber view of the left ventricle (LV), right ventricle (RV) and mitral valve (MV).There is a x-plane through the middle of the heart which shows an orthogonal view of the LV. (b) Mid-esophageal short axis view of the aortic valve (AOV) with interatrial septum (IAS) in view. In this patient, there is pacemaker lead in the right atria (RA). (c) Deep esophageal view showing the right ventricle (RV) and tricuspid valve (TV). (d) 3-dimensional view of the mitral valve. (e) Transgastric view focusing on the right heart with right ventricular outow tract (RVOT and tricuspid valve (TV)

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J. Secor and E. Yucel

Echocardiography forCommon Cardiac Pathologies

Valvular Aortic Stenosis (AS)

• Calcication and/or brosis of the aortic valve which leads to obstruction of

blood ow from the left ventricle into the aorta.

• Typically, the result of one of two pathologies:

– Calcication of a normal trileaet or bicuspid valve (most common cause) – Rhematic aortic aortic stenosis

• Severity of AS is categorized based on the criteria in Table4.1

• Patients with low left ventricular ejection fraction (LVEF) may not have suf-

cient ow to generate high velocity across the aortic valve

• Maximum aortic jet velocity or mean gradient may underestimate severity of AS

in patients low LVEF

• Dimensionless index (DI) can be utilized to aid in diagnosis of severity of AS in

low LVEF.

• DI=velocity time index (VTI) of the left ventricular outow tract/aortic VTI

Aortic Regurgitation (AR)

• Incompetency of the aortic valve results in blood traveling backwards from the

aorta into the left ventricle during diastole

• Typically results from degeneration of the aortic valve leaets or dilation of the

aortic root

• Myxomatous disease (progressive leaet thinning and redundancy) can cause AR

• Endocarditis (infection of the valve) can lead to AR by causing leaet degenera-

tion and/or preventing normal leaet coaptation

• Aneurysmal dilation of the aortic root may lead to insufcient aortic valve coap-

tation and regurgitation

Table 4.1 Aortic stenosis severity classication

Mild Moderate Severe

Vmax (m/s) 2.6–2.9 3.0–4.0 ≥4.0 Mean gradient (mmHg) <20 20–40 ≥40 AVA (cm2) >1.5 1.0–1.5 <1.0 AVAi (cm2/BSA) >0.85 0.6–0.85 <0.6 Dimensionless index >0.5 0.25–0.5 <0.25

Vmax maximum velocity by Doppler, AVA aortic valve area, AVA i indexed AVA; should be only used for patients who has extreme small body habitus, BSA body surface area (m2) Adapted from American Society of Echocardiography guidelines on valve assessment [1, 2]

4 Echocardiography

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Table 4.2 Aortic regurgitation severity classication

Mild Moderate Severe

Regurgitant jet to LVOT ratio (%) <25 25–64 ≥65 Vena contractaa width (cm) <0.3 0.3–0.6 ≥0.6 Regurgitant volume (mL/beat) <30 30–59 ≥60 Regurgitant fraction (%) <30 30–49 ≥50 Regurgitant orice (cm2) <0.1 0.1–0.29 ≥0.3

LVOT left ventricular outow tract Adapted from American Society of Echocardiography guidelines on valve assessment [3]

Width of the regurgitant jet at the orice by color Doppler

Fig. 4.3 Transesophageal view of a patient with rheumatic mitral stenosis. (a) Zoom image of mitral valve from a mid-esophageal view on transesophageal echocardiogram (TEE) of a patient with rheumatic heart disease. There is doming of the anterior mitral valve leaet (white arrow) with almost immobile posterior leaet leading to left ventricular (LV) inow obstruction. (b) 3-D TEE image of mitral valve from the same patient showing fusion of the medial and lateral commissures

• AR can be concomitant with AS when calcied aortic valve leaets neither open

nor close normally

• Severity of AR is characterized by the criteria listed in Table4.2.

Mitral Stenosis (MS)

• MS is restriction of blood ow across the mitral valve that limits ow from the

left atrium into the left ventricle

• Rheumatic heart disease (antibody-mediated inammation of valve secondary to

streptococcus infection) is the most common cause of MS in the developing world

• Commissural fusion, thickening of the mitral valve leaets and chords, doming

of the anterior leaet and immobile posterior leaet are hallmark echocardiographic ndings of rheumatic mitral valve disease (Fig.4.3)

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J. Secor and E. Yucel

• Severe mitral annular calcication (MAC) is a less common cause, which occurs

primarily in elderly patients

• Severity of rheumatic MS is characterized by the criteria listed in Table4.3.

Mitral Regurgitation (MR)

• MR is a failure of the mitral valve leaets to close completely which leads to

backward blood ow from left ventricle into the left atria during systole

• MR is characterized as primary (intrinsic abnormality of the valve leaet tissue)

or secondary (abnormality of the mitral valve annulus or the left ventricle)

• Most common cause of primary MR is mitral valve prolapse followed by endo-

carditis and rheumatic heart disease

• Secondary MR can be caused by coronary artery disease, dilated cardiomyopa-

thy, or long-standing atrial brillation

• Papillary muscle rupture leading to acute severe MR is caused by a myocardial

infarction and is a surgical emergency (Fig.4.4)

• Severity of MR is characterized by the criteria in Table4.4.

Table 4.3 Rheumatic mitral stenosis severity classication

Mild Moderate Severe

Valve area (cm2) >1.5 1.0–1.5 <1.0 Mean gradient (mmHg) <5 5–10 >10 Pulmonary artery mean pressure (mmHg) <30 30–50 >50

Adapted from American Society of Echocardiography guidelines on valve assessment [1]

Severe rheumatic mitral stenosis is dened as a mitral valve area ≤1.5cm2 based on the most

recent ACC/AHA guidelines on management of valvular heart disease [4]

Fig. 4.4 Mitral regurgitation due to papillary muscle rupture. (a) Mid-esophageal long axis view on TEE showing mitral valve in a patient who has papillary muscle rupture. Red arrow shows the papillary muscle that prolapses into the left atria during systole. (b) Same view with color Doppler showing severe eccentric mitral regurgitation (white arrow) during systole. LV left ventricle, AOV aortic valve

4 Echocardiography

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Table 4.4 Mitral regurgitation severity classication

Mild Moderate Severe

Vena contractaa width (cm) <0.3 0.3–0.69 ≥0.7 Regurgitant volume (mL/beat) <30 30–59 ≥60 Regurgitant fraction (%) <30 30–49 ≥50 Regurgitant orice (cm2) <0.2 0.2–0.39 ≥0.4

Adapted from American Society of Echocardiography guidelines on valve assessment [3]

Width of the regurgitant jet at the orice by color Doppler

Fig. 4.5 Tricuspid regurgitation. Apical 4 chamber image on TTE with color Doppler ow which shows severe tricuspid regurgitation. White arrow shows the regurgitant jet

Tricuspid Regurgitation (TR)

• TR is a failure of the tricuspid valve leaets to close completely which leads to

backward blood ow from right ventricle into the right atria during systole (Fig.4.5)

• Like MR, TR has primary and secondary causes

• Etiologies of primary TR include prolapse, endocarditis, carcinoid disease,

injury to the leaets from implantable cardiac devices (i.e., pacemaker leads), trauma, or injury to the leaets during right heart biopsies.

• Secondary TR is more common and can be caused by

– Left sided heart failure – Aortic, mitral, and/or pulmonic valvulopathies – Ventricular septal defect

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