CHAPTER 14 Anesthesia and Cardiac Disease





Introduction


Heart, the pump of the cardiovascular system, often poses challenges to anesthetists during perioperative care when part of its functional capability is lost. Cardiac diseases can range from asymptomatic undiagnosed heart diseases to overtly symptomatic patients with heart failure (HF). So, understanding the pathophysiology of heart diseases and its anesthetic implications are of paramount importance for anesthetists.



Ischemic Heart Disease


A thorough preoperative checkup with possible optimization and an anesthetic management plan modified as per individual patient’s need is critical.



Preoperative Evaluation




  • History: This includes elicitation of the following:




    • History of the last episode of chest pain/myocardial infarction (MI).



    • History of treatment given:




      • Thrombolysis/percutaneous coronary intervention (PCI)/conservative management.



      • Time since the last PCI.



      • Type of stent (bare metal/drug-eluting), number of stents, location.



      • History of previous stent thrombosis.



      • History of adverse cardiac events.



    • Urgency of surgery.



    • Comorbidities: Diabetes/hypertension/congestive HF/renal failure.



    • Current drug regimen the patient is on and any history of irregularities.


Based on the history and presence of risk factors, the probability of major adverse cardiac events (MACE) is calculated as per Lee’s revised cardiac risk index (Box 14.1).



Box 14.1 Lee’s revised cardiac risk index











  • High-risk surgery.



  • Ischemic heart disease (IHD).



  • Congestive heart failure (CHF).



  • Cerebrovascular disease.



  • Insulin-dependent diabetes mellitus.



  • Preoperative serum creatinine concentration > 2 mg/dL.


The presence of two or more risk factors indicates an elevated risk of MACE (>1%).




  • Physical examination:




    • Effort tolerance in terms of metabolic equivalents (METs).



    • General examination.



    • Systemic examination:




      • Respiratory (basal crepitations).



      • Cardiovascular: Murmur, S3 gallop, increased jugular venous pressure.



      • Neurological: Any sign of focal or generalized neurological deficit.



      • Abdomen: Enlarged +/− tender liver.



  • Investigations:




    • Hematological: Complete hemogram, coagulation profile, blood sugar, urea, creatinine, serum electrolytes (if on diuretics) is needed.



    • 12-lead ECG: The presence of q-wave, ST-T changes, obtain ST baseline.



    • Chest X-ray: To rule out cardiomegaly, pulmonary edema.



    • 2D echocardiography with color Doppler: Within last 1 year or since the clinical condition did not change.



    • Exercise testing: Treadmill ECG/dobutamine stress echocardiography.



    • Cardiac CT and MRI.


Other risk calculation scores available are as follows:




  • American College of Surgeons (ACS) National Surgical Quality Improvement Program Myocardial Infarction Cardiac Arrest (NSQIP MICA).



  • ACS NSQIP surgical risk calculator.


Flowchart 14.1 describes the management algorithm after risk stratification as per the 2014 American College of Cardiology (ACC)/American Heart Association (AHA) guidelines.



No Image Available!




Flowchart 14.1 Management after risk stratification—stepwise approach as per 2014 American College of Cardiology (ACC)/American Heart Association (AHA) guidelines. Abbreviation: GMDT, goal directed medical therapy.



Management of Existing Drug Therapy




  • β-blockers: Must not be stopped if already on it; any change in dose or commencement of β-blocker preoperatively should be done 24 hours before to look for the hemodynamic response.



  • Antiplatelets: Aspirin should be continued except in cases of intraocular, intracranial, or spine surgeries; clopidogrel to be stopped 5 days before (however, central neuraxial block [CNB] can be given only after 7 days) and prasugrel to be stopped 7 days before surgery.



  • The rest of the antianginal drugs (nitrates, calcium channel blockers, angiotensin-converting enzyme [ACE] inhibitors) should be continued. ACE inhibitors may be omitted on the morning of surgery to prevent vasoplegia.


Any discontinuation of antiplatelet drugs should be done after consultation with the cardiologist, keeping in mind the risk (stent thrombosis)
versus benefit (intraoperative bleeding) ratio.



Monitoring


The American Society of Anesthesiologists (ASA) standard II monitoring includes:




  • ECG: Lead II for arrhythmia and infarction and lead V5 for ST changes should be on display.



  • Blood pressure (BP): Noninvasive BP (NIBP) and invasive BP may be useful in surgeries that require massive fluid shift, patients with an irregular rhythm, morbidly obese patients, reduced left ventricular (LV) function, and patients requiring frequent arterial blood gas (ABG) analysis for some other reason (e.g., chronic obstructive pulmonary disease [COPD]).



  • Pulse oximetry.



  • End-tidal CO2 monitoring.



  • Temperature monitoring: Prevent hypothermia as shivering can increase oxygen consumption manyfold.


Additional monitoring includes:




  • Central venous pressure (CVP): To assess the preload.



  • Pulmonary artery catheter (PAC): To evaluate the preload for cardiac output measurement and cardiac pacing.



  • Transesophageal echocardiography (TOE): To assess LV function, detection of new regional wall motion abnormality, fluid status.



  • Esophageal Doppler: Goal-directed fluid therapy via descending aorta flow Doppler analysis.



  • Pulse Contour Cardiac Output (PiCCO): For continuous cardiac output measurement, extravascular lung water.



  • Near-infrared spectroscopy (NIRS): For assessment of cerebral and tissue oxygenation.



  • Blood gas analysis: Arterial and mixed venous blood.



Anesthetic Goals


The most important goal is to balance the myocardial oxygen demand and supply ratio.


Increased demand may be due to:




  • Tachycardia: Pain, inadequate depth of anesthesia, arrythmia, withdrawal of β-blocker, hypotension, anemia, and shivering.



  • Increased wall stress: Increased systemic vascular resistance (SVR), increased catecholamines, and increased end-diastolic volume due to bradycardia/fluid overload, aortic stenosis (AS), and concentric hypertrophy.


Decreased supply may be due to:




  • Decreased coronary perfusion pressure: Hypotension, increased left ventricular end-diastolic pressure (LVEDP).



  • Decreased oxygen content of blood: Anemia, hypoxia, hemoglobinopathy.



  • Decreased diastolic time: Tachycardia, nonsinus rhythm.



  • Decreased cardiac output: LV failure.


Other important anesthetic goals include the following:




  • Heart rate (HR) to be kept between 10 and 20% of the baseline value. Tachycardia to be avoided. Bradycardia is dangerous as well.



  • Maintain sinus rhythm. Check for serum electrolytes.



  • Maintain BP between 10 and 20% of the baseline value. Diastolic BP (DBP) is more important in context to coronary perfusion pressure. DBP < 40 mm Hg is poorly tolerated.



  • Adequate analgesia: Reduce catecholamine levels.



  • Maintain an adequate depth of anesthesia.



  • Blood transfusion: Anemia is poorly tolerated due to decreased oxygen-carrying capacity. Keep hemoglobin (Hb) > 10 g/dL.



  • Coagulation: Prevent the hypercoagulable state from reducing stent thrombosis.



  • Temperature: Maintain normothermia.



Anesthetic Management



Choice of Anesthesia



  • Neuraxial block (spinal/epidural/paravertebral block):




    • Advantages: Adequate pain control, avoid stressful airway manipulation.



    • Disadvantages: Hypotension challenging to manage, bleeding risk with antiplatelet agents.



  • General anesthesia (GA):




    • Advantages: Precise control on hemodynamics, no problem with antiplatelet drugs, better to handle emergencies.



    • Disadvantages: Systemic analgesia needed, induction may cause profound hypotension, airway manipulation is associated with severe hemodynamic disturbances, strict vigilance is required.



Premedication

As stress can precipitate MI, premedication with anxiolytics like benzodiazepines is a must. Antisialagogue may be avoided.



Induction

Cardiovascular stability of etomidate makes it an induction agent of choice for cardiac patients. Other intravenous (IV) agents like thiopentone and propofol can be used if hypotension can be avoided. However, ketamine must be avoided due to its sympathomimetic effects. An opioid-based induction with fentanyl/sufentanil may be adopted for patients with compromised LV function. Sympathetic stimulation during laryngoscopy and intubation must be blunted by lignocaine, β-blockers, or opioids.



Neuromuscular Blockade

Vecuronium is ideal due to its cardiovascular stability. Rocuronium may be used for rapid sequence induction and intubation. Atracurium is to be avoided due to its histamine-releasing property. In the case of renal or hepatic failure patients, cisatracurium is the alternative. Succinylcholine should be avoided due to its arrhythmogenic propensity and muscle fasciculation.



Maintenance



  • Nitrous oxide should be avoided for two reasons: It may cause mild sympathetic stimulation, and it is a pulmonary vasoconstrictor.



  • FiO2 should be adjusted to prevent hypoxia.



  • Inhalational agents: All agents are myocardial depressants. Isoflurane causes vasodilation with a theoretical risk of coronary steal syndrome. Sevoflurane causes less hemodynamic perturbation, but cost restricts its widespread use. Desflurane causes cerebral vasodilation and increased sympathetic activity. All inhalational agents are well known for myocardial ischemic preconditioning.



  • Etomidate cannot be used for its antisteroidogenesis effect. The propofol-fentanyl infusion may be an ideal choice. Patients with reduced LV function may be maintained on fentanyl alone.



Reversal

Only glycopyrrolate (no atropine) should be used along with neostigmine. Deep plane extubation is preferred to prevent hemodynamic derangements.



Postoperative Period

The majority of MI occurs in the postoperative period (within 48 h); therefore, all the events which can cause an imbalance between myocardial oxygen demand and supply (chiefly pain) should be avoided in the postoperative period.



Perioperative Myocardial Infarction

Characterized by a rise in troponin I level associated with either cardiac symptoms or ECG changes or supportive imaging.


Two types:




  • Type I—Characterized by acute coronary syndrome (ACS) with sudden erosion of unstable coronary plaque and ECG depicts ST elevation with T inversion and “Q” wave.



  • Type II—Characterized by myocardial demand—supply mismatch and ECG depicts persistent (>30 mins) ST depression.


Tachycardia (HR > 110/min) is the most crucial determinant of perioperative MI; mostly associated with ST-segment depression and are of the non-Q wave type.


If the patient is hemodynamically stable:




  • IV nitroglycerine (the mainstay of treatment).



  • β-blockers.


If the patient is hemodynamically unstable:




  • Treat arrhythmia as per advanced cardiac life support (ACLS) protocol.



  • Intra-aortic balloon pump.



  • Inotrope for circulatory support.



  • PCI angiography and/or angioplasty as early as possible in the postoperative period.



Valvular Heart Disease


The most crucial goal of preoperative assessment is to assess the severity of the valvular lesion. Invasive monitoring is reserved for severe cases of valvular lesions only.



Mitral Stenosis


The most common cause is rheumatic heart disease. The normal mitral valve area is 4 to 6 cm2. Table 14.1 depicts the assessment of severity of mitral stenosis (MS).




Table 14.1 Assessment of severity of MS





























Table 14.1 Assessment of severity of MS

Severity


Mild


Moderate


Severe


Valve area (cm2)


>1.5


1–1.5


<1


Mean gradient across the valve (mm Hg)


<5


5–10


>10


Pulmonary artery systolic pressure (mm Hg)


<30


30–50


>50


Abbreviation: MS, mitral stenosis.


Usually, 20% of diastolic filling occurs during atrial contraction. Being a fixed output disease, perseverance of sinus rhythm and avoidance of tachycardia are essential to maintain cardiac output.



Anesthetic Management



  • Avoid tachycardia: Decreasing the diastole will decrease the LV filling and therefore stroke volume and cardiac output.



  • Avoid hypotension: As these patients have already low cardiac output, hypotension can be detrimental.



  • Avoid a sudden increase in blood volume: Sudden increase in preload with preexisting pulmonary hypertension may cause pulmonary edema and right ventricular (RV) failure.



  • Maintain and avoid a decrease in SVR.



  • Avoid hypoxia, hypercarbia: Hypoxia and hypercarbia by causing pulmonary vasoconstriction can worsen already existing pulmonary hypertension.



Choice of Anesthesia

CNBs should be avoided as hypotension is not acceptable in the already low cardiac output state, and the fluid infusion can precipitate pulmonary edema. However, CNB can be considered for mild-to-moderate lesions by ensuring that significant hypotension is avoided.


As atrial fibrillation is seen in one-third of the patients with MS, a significant number of MS patients will be on oral anticoagulants, contraindicating the use of CNB.



General Anesthesia

Induction: Etomidate, being the most cardiac stable, is the agent of choice.


Maintenance: Isoflurane, being the most cardiac stable, is most preferred; however, sevoflurane and desflurane in lower concentrations can be safely used. Nitrous oxide can cause mild pulmonary vasoconstriction; therefore, it should be avoided.


Relaxant: Vecuronium is the muscle relaxant of choice.


Reversal: As tachycardia is not acceptable, atropine should not be used with neostigmine.



Mitral Regurgitation


Mitral regurgitation (MR) is defined as retrograde blood flow from LV to left atrium (LA) during systole due to multiple mechanisms. Carpentier classification is used for MR. Severe MR is characterized by a vena contracta width ≥ 0.7 and regurgitant volume of ≥ 60 mL/beat.



Anesthetic Management

MR is primarily a systolic event. The regurgitant volume will increase the back pressure in the pulmonary vascular system, causing pulmonary hypertension and also increase the preload of LV, causing volume overload, dilatation of LV, and decreased cardiac output.




  • Avoid bradycardia: HR to be maintained at the normal upper limit (~90 beats/min). Maintain sinus rhythm.



  • Decrease SVR: Increased afterload will increase the regurgitant fraction.



  • Avoid an increase in pulmonary vascular resistance (PVR): Avoid hypoxia, hypercarbia, and acidosis. Avoid Trendelenburg position, check airway pressure during positive pressure ventilation.



  • Contractility: To be maintained at preanesthetic level.



  • Preload: Judicial fluid management to avoid pulmonary edema.



Choice of Anesthesia

As a decrease in afterload decreases the regurgitation, CNBs can be administered. However, excessive hypotension should be avoided.



General Anesthesia

Induction: Etomidate.


Maintenance: Isoflurane. Nitrous oxide is avoided due to pulmonary hypertension.


Muscle relaxant: Vecuronium.



Mitral Valve Prolapse


Generally, mitral valve prolapse (MVP) is a benign condition; however, it can become clinically significant if associated with MR. The hemodynamic principles of management of MVP without MR and with MR are substantially different, for example, increasing LV volume by giving fluids, or by causing bradycardia and hypertension to decrease the degree of prolapse in MVP. On the other hand, the same management strategies will worsen the degree of associated MR when present. Hence, preoperative echocardiography is very useful to identify the presence of associated MR in MVP.


The majority of the MVP cases have a normal ventricular function; therefore, it can be given GA. If GA is to be delivered, then cardiac stable (etomidate, isoflurane, and vecuronium) is preferred.



Aortic Stenosis


AS carries the most dangerous complications among all the valvular heart diseases (angina, syncope, and sudden cardiac death). As much as 75% symptomatic patients with severe AS may die within 3 years without replacement. The normal area of the aortic valve is 2.6 to 3.5 cm2. The severity of AS can be classified as per Table 14.2.


Dec 11, 2022 | Posted by in ANESTHESIA | Comments Off on CHAPTER 14 Anesthesia and Cardiac Disease

Full access? Get Clinical Tree

Get Clinical Tree app for offline access