Heart Diseases and Anesthesia: Part 2 - 2nd Edition

Educational Objectives

Define the pathophysiology of cardiac disease and the implications for the anesthesiologist.

Summary

Heart Diseases and Anesthesia: Part 2

Jochen Steppan, MD, DESA, Assistant Professor, Department of Anesthesiology and Critical Care Medicine, Division of Cardiac Anesthesia, Johns Hopkins School of Medicine, Baltimore, Maryland

Rhythm disorders and conduction defects

Dysrhythmias: unspecific — commonly encountered, caused by ectopic beats (premature atrial or ventricular contractions); premature atrial contractions — originate in atrium, conducted by atrioventricular (AV) node, resulting in narrow complex on electrocardiogram (ECG); premature ventricular contractions — originate in Purkinje fibers of ventricles (rather than sinoatrial node); appear as broad and often misshapen QRS complex on ECG; occurrence — may be seen in healthy adults, but may indicate underlying pathology (eg, ischemia, hypoxia, hypercarbia, catecholamine release, electrolyte abnormalities, thyroid storm); treatment — correct underlying cause, control heart rate

Tachycardia: heart rate >100 beats/minute (bpm); differential diagnosis — broad; may result from intrinsic cardiac problems or in response to extracardiac stimulus; appears as narrow or wide complex on ECG; narrow complex tachycardia — regular or irregular; causes of regular — sinus tachycardia with normal sinus rhythm (eg, resulting from catecholamine release due to pain or anxiety), or reflex tachycardia due to hypertension; other causes — atrial fibrillation (commonly irregular), atrial flutter, AV node re-entry tachycardia, junctional tachycardia, and multifocal atrial tachycardia; wide complex tachycardia — generally considered ventricular tachycardia, but may be combination of narrow complex tachycardia with aberrancy, or result of pacemaker-mediated tachycardia; treatment — elicit underlying problem (blind beta-blocker treatment rarely indicated)

Bradycardia: in adults, commonly defined as heart rate <60 bpm; differential diagnosis — broad; origin — AV block; first-degree AV block — results from prolonged PR interval on ECG beyond 0.2 seconds (most easily seen in ECG lead 2 and often asymptomatic); second-degree AV block — subdivided into Mobitz I (Wenckebach block) and Mobitz II; Mobitz I — results from a block inside AV node; diagnosed by increasingly longer PR interval until QRS complex skipped and P wave not conducted; following conducted P wave begins with shorter PR interval and lengthening repeats; Mobitz II — results from block below AV node; leads to nonconductive P waves without prior prolongation of PR interval; third degree (complete heart block) — occurs as result of AV node or just below it, resulting in complete AV dissociation; no P waves conducted; ventricular response slow; broad escape rhythm; underlying pathology — extrinsic causes (eg, medications, hypoxia, hyperthyroidism, or increased vagal tone), or intrinsic causes (eg, coronary artery disease, ischemia, myocarditis, or surgery); treatment — varies according to symptoms and severity; may be medically managed with atropine, glycopyrrolate, or electric pacing

Cardiac rhythm management devices

Pacemaker

Pacing: accomplished through permanent implantable pacemakers (transvenous, subcutaneous, or epicardial) or temporary pacemaker (transvenous or transcutaneous); permanent transvenous pacemakers — impulse generator and leads, with unipolar, bipolar, or multipolar electrodes and connections in different chambers

Coding system: uses North America Society of Pacing Electrophysiology and British Pacing Electrophysiology Group coding system, comprised of 5 letters; first letter — chamber paced (none, atria, ventricle, or dual); second letter — chamber sensed (none, atria, ventricle, or dual); third letter — mode of response (none, triggered, inhibited, or dual); fourth letter — programmability (none, simple, multiprogrammable, or rate responses); fifth letter — antitachycardia function (none, pacing, shock, or dual); common practice — refer to first 3 letters; pacing ventricle without sensing or emotive response (asynchronous pacing); in dual-dual-dual (most common), pacemaker senses and paces atrium and ventricle using dual response

Indications: generally, may be used in all patients with symptomatic bradycardia not responsive to medication; indications for permanent implantation include sinus node disease, high-grade AV block, long QT syndrome, hypertrophic obstructive cardiomyopathy, and dilated cardiomyopathy

Automated implantable cardioverter defibrillator

Coding system: first letter — chamber shocked; second letter — chamber of antitachycardia pacing; third letter — mode of tachycardia detection (ECG vs hemodynamic); fourth letter — position; primary indications — pace slow heart rate; initiate antitachycardia pacing or shock (in ventricular tachycardia [VT] or ventricular fibrillation); other indications — hypertrophic cardiomyopathy, pre-heart transplant, long QT syndrome, arrhythmogenic right ventricular (RV) dysphasia, Brugada syndrome, decreased ejection fraction for biventricular pacing, and synchronization of right and left heart

Implantation: may be done with moderate sedation in spontaneously breathing patient with face mask

Magnets: used to interrogate device’s battery life and/or pacing thresholds (not for emergency treatment or protection from falsely sensing electrocautery); placement over pacemaker may or may not cause switch to asynchronous mode (depending on manufacturer and device); identify magnet response and battery life prior to operating room

Monitoring: no special monitoring required; turn off ECG artifact to visualize pacer spikes; bipolar electrocautery — minimize or avoid, in favor of monopolar cautery; current return pad should be placed such that electricity does not cross generator heart circuit; after procedure, reprogram device to presurgical settings

Treatment: interventional cardiology with ablation procedures may be used in intermittent VT, re-entry tachycardia, or atrial fibrillation, employing catheter techniques (electricity, laser, temperature, or surgical scarring of atrium); intraoperative evaluation for all arrhythmias includes verifying arrhythmia (palpate pulse, inspect ECG), checking other monitors (blood pressure, saturation, ventilation, volume status), and ensuring hemodynamic stability; if stable, formulate working diagnosis and treat accordingly

Differential diagnoses according to organ systems: tachycardia — iatrogenic (drug side effects, electrocautery), central nervous system (light anesthesia, pain, anxiety, or stroke), cardiac narrow wide complex, respiratory (hypoxia, hypercarbia), metabolic (malignant hyperthermia, sepsis, hypoglycemia, fever), and endocrine (pheochromocytoma, thyroid storm, carcinoid); cardiac causes — differentiating between hypertension, leading to reflex tachycardia, treated by restoring blood pressure first; supraventricular tachycardia regular — possible re-entry tachycardia; treat with vagal maneuver, possibly followed by cardioversion if indicated; supraventricular tachycardia irregular — possible atrial fibrillation; treat with rate control or VT; if patient unstable, immediate cardioversion required; if patient stable, treat with amiodarone

Hypertension: affects estimated 1 billion people worldwide; may be prevalent for a long period, increasing risk for ischemic heart disease, heart failure, renal disease, and cerebrovascular disease (including stroke)

Classifications: primary hypertension (most common) or secondary hypertension (due to defined underlying cause [eg, pheochromocytoma, renal artery stenosis])

Definition: primary hypertension in adults requires systolic ≥120 mmHg, diastolic ≥80 mmHg

Prevalence by age distribution: young adults — isolated diastolic hypertension or combined systolic/diastolic hypertension; older adults — almost exclusively isolated systolic hypertension

Underlying mechanisms: leading causes — narrowing of small arteries, increased vascular stiffness

Treatment: longitudinal; acute lowering of blood pressure during preoperative or perioperative period not necessary except in hypertensive emergency or if other diseases require urgent blood pressure control; severely elevated perioperative blood pressure results in increased perioperative risk and should be investigated; chronic treatment includes lifestyle modifications (diet, exercise) and medication in refractory cases

Pharmacologic therapy: depends on risk profile and comorbidities; classes of drugs — diuretics, calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers, beta-blockers, alpha-blockers, and direct vasodilators

Interactions with anesthetic: diuretics — may lead to electrolyte abnormalities (especially potassium) and volume depletion; hold on morning of surgery unless taken for heart failure; ACE inhibitors and angiotensin-receptor blockers — may lead to refractory hypertension after induction; benefits of giving or holding on day of surgery not definitively proven; beta-blocker and calcium channel blockers — can be associated with bradycardia; beta-blockers should be continued on day of surgery (especially in coronary artery disease); those with hypertension sensitive to negative inotropic and vasodilating effects of anesthetics

Perioperative risk: increased risk, but hypertension itself not good predictor of increased perioperative mortality; recommendations — if hypertension accompanied by other risk factors, treat hypertension well in advance of surgery

Causes of preoperative hypertension: missed dose of medication — administer dose to resolve problem; nervousness or anxiety — requires reassurance; hypertensive crisis — requires treatment; recommendations — if blood pressure ≤180 systolic and ≤110 diastolic, proceed with surgery; however, recommendation not supported by solid data and decisions should be individualized

Intraoperative or postoperative hypertension: diagnose and treat at same time (palpate pulse, check arterial line positioning, repeat cuff measurement); check all monitors (ECG, oxygen saturation, ventilation, temperature, volume status) to ensure hemodynamic stability and adequate level of anesthesia; formulate working diagnosis and treat according; rarely indicated to treat with vasodilators (eg, sodium nitroprusside, nitroglycerin, hydralazine, calcium channel blockers, alpha- or beta-blockers) without first considering differential possibilities

Differential diagnoses according to organ systems: iatrogenic (drug side effects, transducer mount position, wrong cuff size), central nervous system (light anesthesia, pain, anxiety, increased intracranial pressure, autonomic hyperreflexia), cardiac (baseline, hypertension, ischemia, preeclampsia, increased afterload), respiratory (hypoxia, hypercarbia), metabolic (malignant hyperthermia, hypoglycemia, fever), and endocrine (pheochromocytoma, thyroid storm, carcinoid, Cushing syndrome)

Heart failure: major health problem affecting aging population; prevalence — approximately 1 in 100 people >65 years of age (approximately 6 million in United States); 80% of men and 70% of women <65 who have heart failure will die within 8 years

Definition: clinical syndrome characterized by systemic perfusion inadequate to meet metabolic demands as a result of impaired cardiac function; subdivisions — left and/or right heart failure, systolic (associated with reduced myocardial contractility), diastolic (associated with impaired cardiac relaxation and abnormal ventricular filling

Causes: coronary artery disease, hypertension, cardiomyopathy

Diagnostic tools: physical examination (eg, elevated jugular vein pressure), chest x-ray (eg, signs of pulmonary congestion), laboratory data (eg, elevated blood natriuretic peptide)

Algorithms for diagnosis: Framingham criteria (combines major and minor criteria); echocardiogram (aids in subclassification of systolic vs diastolic); ejection fractions — reduced in systolic heart failure; normal in diastolic heart failure (heart failure with preserved ejection fraction), but other abnormal indices can be seen (eg, abnormal E/A ratio)

Classifications: New York Heart Association — focuses on symptoms; class 1: no symptoms with ordinary activity; class 2: symptoms limited to ordinary activity; class 3: exercise limited by symptoms; class 4: symptoms at rest; American College of Cardiology (ACC) and American Heart Association (AHA) — focus on early stages of heart failure; class A: high risk for development of heart failure; class B: asymptomatic heart failure; class C: symptomatic heart failure; class D: refractory end-stage heart failure

Preoperative presentation: cardiac dysfunction on echocardiography, pulmonary congestion, or elevated blood natriuretic peptide

Treatment options: limited; performed according to ACC/AHA classification; class A — modify risk factors with lifestyle modifications; class B — add beta-blockers or ACE inhibitors as indicated; class C — add diuretics or digitalis; class D — may require addition of intravenous inotropes, mechanical circle of support, heart transplant, or hospice

Ventricular assist devices: rapidly expanding field; has greatly improved diagnosis for end-stage heart failure

Treatment in operating room: chronic management uncommon; acute and decompensated heart failure common, necessitating adequate perfusion and oxygen delivery to critical end organs; left-sided heart failure — may benefit from inotropic support (dopamine or epinephrine), especially in low blood pressure; diastolic or systolic heart failure — may benefit from afterload reduction or addition of milrinone or dobutamine; systolic right-sided heart failure — benefits from lowering pulmonary pressures and inotropic support (eg, dobutamine); pulmonary pressures — affected by high partial pressure of oxygen (PO₂), low partial pressure of CO₂ (PCO₂), alkalosis, avoidance of hyperthermia, lowering intrathoracic pressures, blunting catecholamine release, and drugs (eg, inhaled nitric oxide, milrinone, prostaglandins)

Pulmonary edema: accumulation of fluid in lungs

Causes: multiple underlying causes; should be elicited and treated at same time symptoms treated

Classifications: negative pressure pulmonary edema, capillary leak syndrome (eg, eclampsia, low oncotic pressures, or anaphylaxis)

Other considerations: pulmonary embolus, myocardial infarction (MI), heart failure, fluid overload, and aspiration

Clinical presentation: dyspnea, frothy sputum, hemoptysis, anxiety, hypoxia, tachycardia

Diagnostic tools: chest x-ray

Treatment: acute pulmonary edema — often requires immediate treatment of symptoms; depending on level of hypoxia, place patient on 100% oxygen by face mask, continuous positive airway pressure, or bilevel positive airway pressure; if additional intervention required, endotracheal intubation should be undertaken to administer 100% oxygen and positive end-expiratory pressure

Pulmonary hypertension: persistent increase in mean pulmonary artery pressure >25 mmHg at rest; high mortality in patients with concomitant RV failure due to volume overload or RV failure due to ischemia as a result of hypertension

World Health Organization classifications: pulmonary arterial hypertension, pulmonary hypertension associated with left heart disease, pulmonary hypertension associated with lung disease, pulmonary hypertension due to chronic thrombotic disease, and miscellaneous causes

Diagnostic tools: echocardiogram (showing RV and systolic pressure elevated, as measured with Doppler on tricuspid regurgitation jet); technique requires knowledge of current central venous pressure and unobstructed path between RV and pulmonary artery

Treatment: target underlying cause; decrease pulmonary pressures using PO₂, PCO₂, pH, temperature, intrathoracic pressures, catecholamine release, and drug therapy (factors can become worse during perioperative period); periods of hypoventilation may lead to hypoxia and hypercarbia; patients may become acidotic due to mild perfusion and lactate production; hyperthermia common; place on positive pressure ventilation and add positive end-expiratory pressure

Pathways affecting pulmonary artery tone: all pathways can be targeted with specific drugs; nitric oxide pathway — causes vasodilatation and can be provided inhaled as inhaled nitric oxide, intravenous, nitroglycerin, sodium nitroprusside, and indirectly by blocking breakdown of one of its second messages activated by nitric oxide using milrinone; prostacyclin pathway — leads to pulmonary vasodilatation and can be given intravenously or inhaled (eg, iloprost); endothelin pathway — involved in vasoconstriction; endothelin receptor antagonist (eg, bosentan) can be administered

Perioperative treatment of elevated pulmonary pressures: goals — minimize pulmonary pressures to support RV; support or augment RV contractility to overcome high pulmonary pressures; summary — maximize PO₂, decrease PCO₂, keep patient alkalotic, avoid hyperthermia, lower intrathoracic pressure, blunt catecholamine release, and ensure availability of inhaled nitric oxide, milrinone, or prostaglandins

Anesthetic management: general anesthesia — avoids sympathetic surges and hypoventilation, but results in positive pressure ventilation and use of myocardial depressants; sedation — avoids mechanical ventilation but may lead to hypercarbia; neuraxial technique — avoids mechanical ventilation and hypercarbia but may result in anxiety and prereduction for RV; prudent to favor inotropic support (eg, milrinone, epinephrine) over pure vasopressor support (especially phenylephrine); avoid large fluid boluses; have contingency plan for pulmonary vasodilators (eg, inhaled nitric oxide) or more invasive therapy

Cardiogenic shock: extreme form of inadequate end-organ perfusion of cardiac origin that leads to insufficient delivery of oxygen to tissues, resulting in low cardiac output, local hypoxia, and nutrient starvation, which leads to ischemia and cell death

Clinical presentation: hypotension, low cardiac index, and end-organ malperfusion, manifested by oliguria, cool extremities, weak pulse, and altered mental status (despite adequate intravascular volume and normal or high cardiac filling pressures)

Causes: left ventricular failure — due to MI; patients presenting with ST elevation MI have 5% to 8% chance for deterioration to cardiogenic shock; other causes — papillary muscle rupture, myopericarditis, Takotsubo cardiomyopathy, acute valvular insufficiency, aortic dissection, cardiac tamponade, pulmonary embolism, and arrhythmias

Diagnostic tools: pulmonary artery catheter and echocardiography

Treatment: maintain adequate volume status and pharmacologic support; inotropic agents (preferably low dose); no single inotrope preferred over others; pharmacologic therapy — epinephrine, norepinephrine, and dobutamine; adjunct therapy may include dopamine, vasopressin; intra-aortic balloon pump — often needed in addition to pharmacologic therapy to improve coronary perfusion pressure by augmenting diastolic blood pressure in aortic root; afterload-reducing effect of pump likely of much less effect; other treatments — ventricular assist device, extracorporeal membrane oxygenation, or heart transplant

Cardiac transplantation: most effective treatment for heart failure refractory to medical or surgical therapy

Risk factors: hypertension, diabetes, coronary artery disease, and MI

Etiology: non-ischemic cardiomyopathy (most common) and ischemic cardiomyopathy

Anesthetic management: minimize ischemic time; place arterial line prior to induction; ensure hemodynamic stability

Techniques: balance technique; recent shift from bi-atrial approach

Denervated hearts: hearts denervated with no sensory, sympathetic, or parasympathetic connections (due to prior heart transplantation); lack of parasympathetic tone (lowering heart rate at baseline) results in a higher-than-expected heart rate (90-100 bpm); stroke volume cannot increase (due to direct sympathetic stimulation), and depends on circulating catecholamines and adequate preload

Pharmacologic therapy: administer direct-acting agents (eg, isoproterenol, epinephrine, or norepinephrine); external or internal pacing may be performed

Cardiac tamponade: accumulation of pericardial fluid or blood leads to impaired ventricular filling and low cardiac output

Causes: variety of causes lead to fluid accumulation in pericardial sac

Underlying pathology: trauma, ascending aortic dissection, cardiac surgery, MI (complicated by ventricular rupture), lung cancer, pericarditis, radiation therapy, or central line placement

Symptoms: unspecific; may be associated with chest pain and its differential diagnosis

Clinical signs: Beck’s triad — hypertension, jugular venous distension, and muffled heart sounds; pulsus paradoxus — not specific; can occur with other diseases (eg, pericarditis, sleep apnea, or chronic obstructive pulmonary disease); other signs — low voltage on ECG

Diagnostic tools: chest x-ray and echocardiography (transesophageal can be used to visualize amount of pericardial fluid around heart, atrial or ventricular compression, and dynamic shift of ventricular septum); arterial line (demonstrating hypertension, pulsus paradoxus), and pulmonary artery catheter (equalization of pressures in heart, with progressing tamponade, central venous pressure, pulmonary artery pressures, and wedge pressure converging on the same number as flow across heart diminishes)

Treatment: depending on severity, subxiphoidal percutaneous drainage or pericardial window; goal — maintain contractility, heart rate, and afterload

Anesthetic management: subcutaneous drainage can be performed with local anesthesia; general anesthesia not needed except for local (and perhaps small amount of ketamine in severely compromised patient); no single drug regimen best

Constrictive pericarditis: leads to impaired ventricular filling due to inflammatory process of pericardium that results in pericardial fibrosis without emergent presentation

Causes: infection (eg, tuberculous, bacterial), inflammatory and autoimmune (post-viral or post-MI), miscellaneous (due to radiation or neoplastic infiltration); all causes lead to thickened, calcified, and increasingly fibrosed pericardium; leads to ventricular filling impairment (but contrary to tamponade, presentation less acute and more difficult to determine)

Symptoms: consistent with heart failure, dyspnea, fatigue, and lower extremity edema; increased jugular venous pressure, edema, and hepatomegaly

Diagnostic tools: echocardiography (most common), imaging modalities (eg, chest x-ray), computed tomography scan, and cardiac catheterization (least common)

Treatment: surgical pericardiectomy (pericardial stripping) — used especially with advanced constrictive pericarditis; commonly performed by median sternotomy to remove entire pericardium; hemodynamic goals — maintain heart rate, afterload, and myocardial contractility while maintaining adequate preload

Monitors: arterial or central lines

Pharmacologic therapy: not important which drugs are used as long as hemodynamic goals are met

Readings

Disclosures

Acknowledgements

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

ANBR150135

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.

More Details - Certification & Accreditation