Stages of Heart Failure

Reproduced from Jessup M, Abraham WT, Casey DE, et al. 2009 Focused update: ACCF/AHA guidelines for diagnosis and management of heart failure in adults. J Am Coll Cardiol 2009;53:1343–1382, with permission.

4) Symptoms

    a) Nonspecific symptoms include dyspnea at rest or on exertion, easy fatigability, and peripheral edema.

    b) More specific signs (but not necessarily specific) include orthopnea, paroxysmal nocturnal dyspnea, jugular venous distention, cardiac enlargement, and a third heart sound (5).

5) Evaluation

    a) Defining whether the patient has preserved or reduced left ventricular function (as determined by ejection fraction) has significant implications with two entities being important to differentiate: heart failure with reduced ejection fraction (HFREF) and heart failure with normal ejection fraction (HFNEF).

    b) Diagnostics. Consider the following tests in patients with suspected HF:

  i) Routine electrocardiography

  ii) Chest x-ray with a focus on pulmonary edema or possible cardiomegaly

  iii) Plasma concentrations of natriuretic peptides

(1) Natriuretic peptides (e.g., b-type or brain natriuretic peptides—BNP and NT-proBNP—N-terminal fragment of prohormone of BNP) are elevated in the presence of left ventricular failure.

(2) Sensitivity may be impaired in the presence of obesity (6)

(3) Other causes of increased BNP include ventricular hypertrophy, volume expansion, decreased renal clearance, hypoxia, tachycardia, and female gender (7).

  iv) Transthoracic echocardiography—two-dimensional echocardiography with Doppler to assess left ventricular ejection fraction, left ventricular size, wall thickness, and valve function (4)

    c) Based on the 2007 American College of Cardiology/American Heart Association Guidelines (8), it is clear that one must answer the following question prior to proceeding to the operating room. “Are the symptoms of heart failure new?”

  i) If so, elective surgical procedures should be postponed until optimization has occurred.

  ii) The patient who has a known history of HF but worsening symptoms (i.e., decompensation) should also have elective surgery delayed.

6) HF with reduced ejection fraction

The perioperative management of patients with HFREF can be quite complex. There are several important implications for the anesthetic care.

    a) Medical management of the patient with HFREF

  i) Diuretic therapy

  ii) β-adrenergic antagonists used judiciously

  iii) Angiotensin converting enzyme (ACE) inhibitors, or angiotensin II receptor blockers (ARBs), in patients who are ACE inhibitor intolerant

  iv) For African Americans, guidelines suggest the addition of hydralazine and nitrates for refractory symptoms (4)

  v) Hospitalized patients with HFREF may be on more powerful vasodilators or inotropic medications such as:

(1) Vasodilators: nitroglycerin, nitroprusside, or nesiritide with the goal of decreasing left ventricular filling pressures (LVFP) (9)

(2) Inotropes: dobutamine and milrinone have the benefit of not only lowering the LVFP but also increasing cardiac output.

  vi) Avoid calcium channel blockers due to their negative inotropic qualities.

  vii) Avoid nonsteroidal anti-inflammatory agents due to their potential to aggravate the cardiorenal syndrome commonly seen in this patient population.

    b) Implantable cardioverter-defibrillator (ICD) is indicated for all patients with: (4)

  i) Nonischemic dilated cardiomyopathy

  ii) Ischemic heart disease at least 40 days post MI

  iii) LVEF ≤ 35%

  iv) History of cardiac arrest/ventricular fibrillation/ventricular tachycardia

  v) Life expectancy of >1 year

    c) Cardiac resynchronization therapy (CRT)

  i) Playing a growing role in the management of HFREF.

  ii) CRT addresses dyssynchronous contraction commonly found in HFREF by activating the right and left ventricular chambers via a biventricular pacemaker and is at times combined with ICD therapy.

    d) Anesthetic implications in patient with HFREF (Table 60-2)

1) Invasive monitoring

(1) Arterial BP or central pressure monitoring may be indicated

(2) Surgical risk should guide the choice of monitors selected. For low risk procedures (e.g., ambulatory-based such as hernia repairs, cystoscopies, and cataract surgery), requires no invasive devices; intermediate- to high-risk surgery requires more intensive monitoring

(3) Pulmonary artery catheters are not routinely recommended for all HFREF patients presenting for noncardiac surgery (11).

2) Inhalational anesthetics

(1) Cause a dose-dependent decrease in cardiac output and cardiac contractility

(2) Nitrous oxide, though having the benefit of allowing lower concentrations of inhaled agents to be administered, is also associated with myocardial depression in the presence of HF, especially when administered with opioids.

(3) Nitrous oxide may have a deleterious effect on the pulmonary vascular resistance, causing an increase in right atrial pressures secondary to sympathetic stimulation (12).

7) HF with normal ejection fraction

Approximately 50% of HF patients have poor systolic function (13), the rest of the patients presenting with HF will have what is known as HFNEF. These patients are likely to be older women with HTN.

    a) Symptoms and signs

  i) Clinical signs consistent with HF as mentioned previously, notably shortness of breath

  ii) Preserved ejection fraction on echocardiographic exam

  iii) Increased filling pressures and impaired left ventricle (LV) filling

    b) Pathophysiology of HFNEF

  i) Patients with HFNEF have a normal ejection fraction, but have diastolic dysfunction (DD), a hallmark of HFNEF

  ii) DD is a result of both impaired relaxation and increased LV passive stiffness, and may be part of the normal aging process (14).

  iii) Impaired relaxation is likely due to ineffective calcium removal from the cytosol resulting in a slow LV isovolemic relaxation phase, which is worsened by myocardial ischemia.

  iv) The net result of the impaired relaxation and increased stiffness is an elevated left ventricular end diastolic pressure, which can translate to an increase in left atrial pressure as well as pulmonary capillary pressure.

  v) In HFNEF, an increase in blood volume coupled with tachycardia-induced decreased diastolic filling time can cause dyspnea on exertion and pulmonary edema (seen in response to exercise).

  vi) Noncompliant LV is unable to accept more preload and thus is unable to use the Frank-Starling mechanism to augment stroke volume (15).

    c) Medical management of HFNEF

In contrast to HFREF, evidence is lacking for any specific therapy to reduce mortality in patients with HFNEF (16–19). The 2005 ACC/AHA guidelines do offer some recommendations for treatment of HFNEF (20). Main therapeutic goals include:

  i) Avoid tachycardia

  ii) Avoid ischemia

  iii) Avoid HTN

    d) Medication recommendations

  i) β-Adrenergic antagonists and/or calcium channel blockers have value in that they both help reduce heart rate, improve diastolic filling time, decrease BP, and decrease myocardial ischemia.

  ii) ACE inhibitors/ARBs in addition to decreasing afterload may help in the regression of myocardial fibrosis (21).

    e) Anesthetic implications of HFNEF Table 60-2

1) Preoperatively

(1) Up to 61.5% of geriatric surgical patients exhibit evidence of abnormal diastolic filling, DD and HFNEF (22).

(2) Patient must be medically optimized by addressing uncontrolled HTN, atrial fibrillation, HF, or myocardial ischemia.

(3) Patients should continue their cardiac medications the day of surgery to avoid HF exacerbations.

2) Intraoperative

(1) Standard ASA monitors are usually all that is required for the patient with HFNEF.

(2) The decision for invasive monitoring should be individualized and take into account the anticipated surgical stress, anticipated volume shifts, and comorbidities.

(3) IV and inhalational anesthetic agents

   (a) Both can adversely affect cardiac diastolic function (23)

   (b) Maintaining hemodynamic parameters seems to be more important than avoiding certain anesthetic agents

   (c) In fact, diastolic function may actually improve after induction of general anesthesia (24).

(4) Avoid tachycardia since it shortens diastolic filling time

(5) Blood pressure should be maintained within 10% of baseline since HTN can impede ejection, exacerbate ischemia, and increase LV volume, whereas hypotension, especially diastolic hypotension, can cause a decrease in coronary perfusion pressure resulting in ischemia

(6) Avoid hypercarbia and hypoxia, both of which may exacerbate any preexisting pulmonary HTN

(7) Close management of volume status is mandatory since patients are very sensitive to alterations in preload

(8) Key point. General or regional anesthetic induced venodilation may decrease venous return and preload. Caution is advised, however, in indiscriminately administering fluid because upon emergence, venous return is restored and this may precipitate pulmonary edema or atrial fibrillation.

1) Postoperative

(1) Patients with HFNEF should be observed closely in the early postoperative period.

(2) Volume overload may occur not only in the postanesthesia care unit, but around postoperative day 3 as any third spaced fluid is reabsorbed.

(3) Pain control is important to limit tachycardia and HTN.

Chapter Summary for Key Anesthetic Considerations for HFREF and HFNEF

HF, heart failure; HFNEF, heart failure with normal ejection fraction; HTN, hypertension.

 

References

1. Lloyd-Jones D, Adams RJ, Brown TM, et al. Heart disease and stroke statistics 2010 update. A Report From the American Heart Association. Circulation 2010;121:e46–e215.

2. Levy D, Larson MG, Vasan RS, et al. The progression from hypertension to congestive heart failure. JAMA 1996;275:1557–1562.

3. Frankel DS, Vasan R, D’Agostino RB Sr, et al. Resistin, adiponectin, and risk of heart failure the Framingham offspring study. J Am Coll Cardiol 2009;53:754–762.

4. Jessup M, Abraham WT, Casey DE, et al. 2009 Focused update: ACCF/AHA Guidelines for Diagnosis and Management of Heart Failure in Adults. J Am Coll Cardiol 2009;53:1343–1382.

5. Mant J, Doust J, Roalfe A, et al. Systematic review and individual patient data meta-analysis of diagnosis of heart failure, with modeling of implications of different diagnostic strategies in primary care. Health Technol Assess 2009;13:1–207.

6. Maisel A, Mueller C, Adams K Jr, et al. State of the art: using natriuretic peptide levels in clinical practice. Eur J Heart Fail 2008;10:824–839.

7. Omland T Advances in congestive heart failure management in the intensive care unit: B-type natriuretic peptides in evaluation of acute heart failure. Crit Care Med 2008;36(1 suppl):S17–S27.

8. Fleisher LA, Beckman JA, Brown KA, et al. ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery: Executive Summary. Circulation 2007;116:1971–1996.

9. Gheorghiade M, Pang PS. Acute heart failure syndromes. J Am Coll Cardiol 2009;53:557–573.

10. Zaidan JR, Atlee JL, Belott P, et al. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverter-defibrillators. Anesthesiology 2005;103:186–198.

11. Vincent JL, Pinsky MR, Sprung CL, et al. The pulmonary artery catheter: In medio virtus Crit Care Med 2008;36:3093–3096.

12. Stoelting RK, Hillier S Chapter 2: Inhaled Anesthetics. Pharmacology & Physiology in Anesthetic Practice. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006:42–86.

13. Owan TE, Hodge DO, Herges RM, et al. Trends in prevalence and outcome of heart failure with preserved ejection fraction. N Engl J Med 2006;355:251–259.

14. Zile MR, Baicu CR, Gaash WH. Diastolic heart failure-abnormalities in active relaxation and passive stiffness of the left ventricle. N Engl J Med 2004;350:1953–1959.

15. Kitzman DW, Higginbotham MB, Cobb FR, et al. Exercise intolerance in patients with heart failure and preserved left ventricular systolic function: failure of the Frank–Starling mechanism. J Am Coll Cardiol 1991;17:1065–1072.

16. Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction: the CHARM-Preserved Trial. Lancet 2003;362:777–781.

17. Ahmed A, Rich MW, Fleg JL, et al. Effects of digoxin on morbidity and mortality in diastolic heart failure: the ancillary digitalis investigation group trial. Circulation 2006;114:397–403.

18. Cleland JG, Tendera M, Adamus J, et al. The perindopril in elderly people with chronic heart failure (PEP-CHF) study. Eur Heart J. 2006;27:2338–2345.

19. Massie BM, Carson PE, McMurray JJ, et al. Irbesartan in patients with heart failure and preserved ejection fraction. N Engl J Med 2008;359:2456–2467.

20. Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 Guideline Update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association task force on practice guidelines (writing committee to update the 2001 guidelines for the evaluation and management of heart failure): developed in collaboration with the American College of Chest Physicians and the International Society of Heart and Lung Transplantation: endorsed by the Heart Rhythm Society. Circulation 2005;112:e154–e235.

21. Diez J, Querejeta R, Lopez B, et al. Losartan-dependent regression of myocardial fibrosis is associated with reduction of left ventricular chamber stiffness in hypertensive patients. Circulation 2002;105:2512–2517.

22. Phillip B, Pastor D, Bellows W, et al. The prevalence of preoperative diastolic filling abnormalities in geriatric surgical patients. Anesth Analg 2003;97:1214–1221.

23. Pagel PS, Grossman W, Haering JM, et al. Left ventricular diastolic function in the normal and diseased heart. Anesthesiology 1993;79: 1104–1120.

24. Couture P, Denault AY, Shi Y, et al. Effects of anesthetic induction in patients with diastolic dysfunction. Can J Anesth. 2009;56:357–365.

Cardiomyopathy

Gurdev Rai, MD

1) Epidemiology and pathophysiology

    a) Hypertrophic cardiomyopathy (HCM) occurs at a rate of 1:500 in the adult population of the United States and is characterized by a large, nondilated left ventricle (LV) (1). This characteristic must exist in the absence of any other known causes of LV hypertrophy. The causes of HCM are both genetic and nongenetic.

  i) The nongenetic form is usually seen in athletes and is a milder hypertrophy.

  ii) The genetic form is due to mutations in one of up to 11 genes and thus, results in large amounts of clinical variability (3).

  iii) Pathophysiology

(1) The hypertrophic LV becomes harder to fill passively, resulting in diastolic dysfunction.

(2) The hypertrophic muscle requires more oxygen to function, making it prone to ischemia (3).

(3) In cases involving hypertrophy of the interventricular septum, dynamic left ventricular outflow tract obstruction can pose a unique challenge to the anesthesiologist.

    b) Dilated cardiomyopathy (DCM) has a prevalence of 1:20,000 in the middle-aged population and is characterized by ventricular dilation secondary to toxic, metabolic, or infectious causes leading to myocyte damage (1).

  i) Etiologies include viral or alcohol-related myocyte degeneration with a pattern of irregular myocyte hypertrophy and atrophy. Histologically, one also sees perivascular and interstitial fibrosis.

(1) Viral DCM is most common in young, previously healthy individuals subjected to coxsackie B or echovirus.

(2) Alcohol-related DCM results from chronic ingestion and is most often reversible.

    c) Restrictive cardiomyopathy (RCM) is the least common and defined by impaired ventricular filling of normal sized ventricles. This is usually due to a fibrosed or scarred endomyocardium. Causes include:

  i) Deposition of abnormal substances like amyloid, iron, glycogen, or tumor.

  ii) Scarring related to anthracycline toxicity, radiation, or endomyocardial diseases such as hypereosinophilic syndrome.

  iii) Recently, scientists are describing a genetic component to RCM as well (1).

    d) Arrythmogenic right ventricular cardiomyopathy (ARVD) is defined by a segmental loss of right ventricular myocytes. This is noticeable as segmental wall motion abnormalities of the right ventricle on echocardiography.

  i) Death in ARVD occurs secondary to arrhythmia related sudden death or eventual right heart failure. Its prevalence in this country is 1:10,000 (4).

  ii) Histologically, one sees the displacement of normal cardiac tissue with adipocytes or fibrous tissue.

  iii) Genetic disease with autosomal dominant inheritance and variable penetrance.

2) Signs and symptoms

    a) The normal heart can be described as a pump consisting of four chambers with an intrinsic electrical system.

    b) There are two systems of interest in a normally functioning heart, the mechanical and the electrical.

1) These systems are dependent on each other to provide baseline functioning of the heart.

2) In times of stress, the two systems must have adequate reserves to meet the body’s demands.

1) Cardiomyopathies result from a defect in the mechanical system associated with decreased cardiac performance.

    c) Systolic failure

  i) As remodeling of the ventricular structure progresses, the associated changes in the mechanics of the heart eventually start impacting the heart’s functional reserve.

  ii) Systolic failure occurs more often in DCM.

  iii) Increased end-diastolic volume and decreased ejection fraction result in signs of decreased O₂ delivery. The body tries to compensate by increasing heart rate and increasing vascular tone.

  iv) Thus, with DCM the classical signs of systolic heart failure including cyanosis, cold extremities, and decreased exercise tolerance are observed.

    d) Diastolic dysfunction

  i) With HCM and RCM a combination of systolic and diastolic dysfunction is observed.

  ii) The decreased compliance of the LV results in increased filling pressures, increased left ventricular end diastolic pressure, and decreased end-diastolic volume.

  iii) The left atrium may hypertrophy and eventually dilate, increasing the risk of atrial fibrillation or flutter; further decreasing the end-diastolic volume in a very preload dependent ventricle.

  iv) Clinically, the body compensates with tachycardia and increased systemic vascular resistance.

  v) Symptoms include dyspnea upon exertion, pulmonary edema, atrial fibrillation, and vascular congestion/edema.

    e) Arrhythmias

  i) A dilated or hypertrophic heart may have impaired conduction of electrical impulses.

  ii) Commonly, patients exhibit bundle branch blocks, first-degree heart blocks, and an increased incidence of tachyarrythmias (5).

  iii) Sudden death is a constant threat to all patients with cardiomyopathy (2).

    f) Left Ventricular Outflow Tract Obstruction. With HCM, one must pay special attention to left ventricular outflow tract obstruction.

  i) Symptoms/signs include

(1) Fainting spells and angina during stressful situations or conditions, which increase preload.

  ii) A dynamic holosystolic murmur is typically heard on ascultation.

  iii) Echocardiographic imaging usually shows a large interventricular septum.

(1) As flow increases, the septum and mitral valve leaflet get pulled together based on the Bernoulli Effect. This causes an obstruction of the outflow tract during systole.

  iv) During anesthesia, any stimulus, which increases contractility or preload, can cause hypotension and heart failure in these patients.

1) Treatment options depend primarily on the cardiomyopathy classification

    a) Lifestyle modifications such as weight control, abstinence from tobacco, and moderation of alcohol intake.

    b) Pharmacotherapy

  i) Emphasis is on ACE-inhibitors, potassium sparing diuretics, vasodilators, and digitalis, all of which prevent further remodeling of the heart.

  ii) In addition, the antiarrhythmogenic therapy is employed.

  iii) In patients with severe dysfunction, warfarin is utilized to decrease the viscosity of blood and encourage flow. It also prevents the formation of clot in a low flow state.

  iv) The definitive treatment is cardiac transplantation. In patients who are not candidates for transplantation or those on the waiting list, ventricular assist devices can be used.

4) Anesthetic implications

    a) Preoperative considerations

  i) One must define the type of cardiomyopathy present and the patient’s functional status.

  ii) The physical exam includes a thorough heart and lung exam.

  iii) If the patient has signs of heart failure, the surgery should be delayed until further workup including chest films, ECG, and echocardiogram can be obtained (6).

  iv) In emergent situations, the goal is to maintain normal hemodynamics with the aid of invasive monitors.

  v) An arterial line and a central venous pressure line are the minimum to provide a safe anesthetic in a patient with an unknown cardiomyopathy

  vi) Preparedness for arrhythmias, cardiac arrest, and potentially death is absolutely relevant to the perioperative care of these patients. This must be discussed with the patients as well as the care team.

    b) Intraoperative

  i) Hypertrophic Cardiomyopathy (HCM)

(1) Typically, these patients are on β-adrenergic antagonists or amiodarone and may even have an implanted defibrillator. One must ensure that the patient has had all scheduled medications. The defibrillator must be turned off if interference from surgical devices like unipolar electrocautery is expected and external defibrillating equipment must at hand.

(2) The main goals to help prevent obstructive physiology are: maintain preload and afterload, maintain a relatively slow sinus rhythm, and recognize undiagnosed obstruction (6).

(3) Afterload and preload are maintained with heart rate control and maintenance of systemic vascular resistance during induction, maintenance, and emergence from anesthesia.

(4) Junctional rhythms are not tolerated well due to the dependence of the left ventricular end diastolic volume on atrial kick. Early detection and treatment of a junctional rhythm is imperative.

(5) Sudden hypotension and a dynamic systolic murmur should raise the suspicion of undiagnosed LV outflow obstruction. In these cases, drugs that increase heart rate or contractility should be avoided. Emphasis should be on filling the ventricles and slowing the heart rate. This can be accomplished with fluid boluses, phenylepherine, and beta-blockade.

  ii) Restrictive Cardiomyopathy (RCM)

(1) Initially, try to determine the levels of venous congestion by looking for jugular venous distension, hepatojugular reflex, or peripheral edema.

(2) In patients with evidence of congestion, diuretics are the preferred treatment.

(3) One must also be wary of arrhythmias. Antiarrhythmogenic treatment with beta-blockers or amiodarone is the mainstay.

(4) Preoperative echocardiographic studies are essential to define the level of diastolic dysfunction.

(5) Restrictive hearts are rate-dependent for cardiac output. Thus, rate control and maintenance of sinus rhythm are keys to a safe anesthetic (6).

  iii) Dilated Cardiomyopathy (DCM)

(1) Hemodynamic goals of maintaining preload and sinus rhythm should be accomplished by avoiding myocardial depression and preventing large increases in afterload.

(2) Careful induction using a technique that preserves myocardial contractility, preload, and rhythm (6).

(3) Moderately elevated heart rates are better tolerated since they prevent large increases in end-diastolic volume. Therefore, drugs like ephedrine, epinephrine, and dopamine become the treatments of choice for hypotension.

  iv) Arrythmogenic right ventricular cardiomyopathy (ARVD)

(1) The main goal in patients with ARVD is to promote forward flow out of the right side of the heart. This depends on balancing adequate preload with the myocardium’s ability to contract.

(2) A pulmonary artery catheter (PAC), or transesophogeal echocardiography, is indicated in intermediate- to high-risk procedures. However, one must be ready to handle any potential malignant arrhythmia associated with PAC placement or anesthesia administration.

(3) Familiarity with AICDs and antiarrhythmia medications is essential.

(4) Afterload reduction by maintaining low pulmonary vascular resistance and left ventricular function are also imperative. The emphasis must be on maintaining normocapnea, preventing hypoxia or acidosis to minimize changes in pulmonary vascular resistance (4).

    c) Postoperative care depends on the operation

  i) For minor procedures, it may be adequate to monitor in a telemetry or stepdown unit. For moderate- to high-risk surgery, intensive care settings are the safest.

  ii) Restarting the patient’s preoperative medications in a timely fashion is critical.

  iii) For patients with AICDs that were turned off, trained personnel must be available to reprogram the device after surgery. If not, one must keep a defibrillator at hand and monitor the patient closely for malignant arrhythmias (5).

5) Follow-up

    a) Cardiologists should be alerted to, if not involved with, these patients prior to the operative day and informed of any perioperative events.

    b) The patient should be evaluated to ensure that their medications have been restarted and that their AICD is functional.

    c) If any clinical signs of decompensation are evident, an evaluation of cardiac function involving an echocardiogram must be pursued, with any changes worked up as potential myocardial infarction or a need to further optimize medications.

HCM, hypertrophic cardiomyopathy; DCM, dilated cardiomyopathy.

References

1. Maron BJ, Towbin JA, Thiene G, et al. Contemporary Definitions and Classifications of the Cardiomyopathies: An American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure, and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation 2006;113:1807.

2. Elliot P, Anderson B, Arbustini E, et al. Classification of the Cardiomyopathies: a position statement from the European Society of Cardiology Working Group on Myocardial and Pericardial Disease. Eur Heart J 2008;29:270.

3. Neubauer S. The failing heart-an engine out of fuel. N Engl J Med. 2007;356:1140–1151.

4. Alexoudis AK. Anaesthetic implications of arrhythmogenic right ventricular dysplasia cardiomyopathy. Anaesthesia 2009;64:73–78.

5. Practice advisory for the perioperative management of patients with cardiac rhythm management devices: pacemakers and implantable cardioverters-defibrillators; a report by the American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Anesthesiology 2005;103:186–198.

6. Stoelting R, Dierdorf S. Anesthesia and Coexisting Disease. 4th ed. Philadelphia, PA: Churchill Livingstone; 2002.

Pulmonary Hypertension

Nathaen Weitzel, MD

1) Definitions and etiology

    a) PH is defined as a syndrome with elevated pulmonary artery pressures (mean PAP > 25 mm Hg at rest) (1–3).

    b) PH is associated with reduced nitric oxide (NO) and prostacyclin synthesis as well as with increased thromboxane production (4).

  i) Histologic features include medial thickening and intimal fibrosis(5).

    c) Classically, PH was described as primary or secondary PH. In 1998, the World Health Organization adopted a new classification system describing five categories of PH:

  i) Isolated pulmonary arterial hypertension (PAH)

(1) Includes primary PH, systemic to pulmonary shunts and collagen vascular disease

(2) PAH is defined as exclusion of secondary causes, elevated mean PAP (>25 mmHg), and elevated PVR of >3 Woods units

  ii) PAH associated with diseases of the respiratory system and/or hypoxia

(1) Includes chronic obstructive pulmonary disease, obstructive sleep apnea

  iii) Pulmonary venous hypertension

(1) Includes mitral valve disease, chronic left ventricle [LV] dysfunction

  iv) PH associated with chronic embolic/thrombotic disease

  v) PH attributed to direct obstruction of the pulmonary vasculature (inflammatory pulmonary capillary hemangiomatosis) (1)

2) Pathophysiology

    a) Acute changes

  i) The normal pulmonary vascular resistance (PVR) is <90% of the systemic vascular resistance (SVR).

  ii) Because the right ventricle (RV) is designed for a low pressure system, an acute increase in pulmonary pressure often results in rapid right ventricular failure (i.e., acute pulmonary embolus, acute severe MR) (1,5).

    b) Chronic PH

  i) PH tends to develop over time, allowing the RV to compensate for the increased work via hypertrophic changes.

  ii) Unfortunately, the RV has limited ability to compensate in this manner and will eventually dilate and fail. RV failure leads to a variety of events including (1,5)

(1) Reduced RV stroke volume, decreased preload to the LV, and resultant hypotension

(2) Intraventricular septum of the dilated RV shifts toward the LV, further decreasing LV output.

(3) Reduced RV coronary blood flow secondary to disruption of the normal systolic and diastolic coronary blood flow pattern

  iii) Right-to-left shunt may develop in patients with a patent foramen ovale (~30% of adults) resulting in hypoxia.

1) Surgical and anesthetic risks

    a) PH patients are high-risk surgical candidates.

  i) Published series demonstrate a range of surgical mortalities from a low 4% to high of 24% depending on disease severity and surgical procedure (1).

  ii) Surgical and anesthetic risk should be clearly stated to the patient, especially for an elective case.

    b) Hemodynamic spiral

  i) Acute deterioration is possible as RV failure causes reduced pulmonary blood flow, leading to hypoxia, which subsequently increases the PVR.

  ii) The elevated PVR ultimately leads to increased strain on the RV.

  iii) This initiates a catastrophic hemodynamic chain of events where the decreased RV stroke volume decreases LV output and coronary blood flow decreases to both the LV and RV.

  iv) The already failing RV may not be able to recover from this, resulting in cardiac arrest. This “death spiral” is always a potential in PH patients; the anesthesia provider should be aware of it and take steps to prevent it.

4) Preoperative evaluation

    a) Patients with PH are high-risk patients who should be evaluated by a PH specialist before surgery and should be started on appropriate medication as indicated.

    b) The goal of the pre-op evaluation is to determine if the patient suffers from PH, RV failure, or a combination of these, as this knowledge affects management (5).

    c) Clinical findings

  i) The signs of PH are often vague, but the most common sign is dyspnea with exertion.

  ii) This symptom can progress to dyspnea at rest, chest pain, fatigue, and syncope. A history of syncope is an extremely poor prognostic sign (1).

    d) The etiology of the PH should be determined if possible, and a cardiac echocardiographic exam should be obtained (1,5).

  i) Valvular structures, size and function of both RV and LV, and the presence of any intracardiac shunts should be evaluated.

  ii) Echocardiography can measure mean PAP; however, this is often underestimated; therefore, cardiac catheterization is the gold standard of measure.

    e) Pulmonary vascular reactivity can also be determined at catheterization to test responsiveness to vasodilators.

    f) Medications

  i) Common medications for the treatment of PH include calcium channel blockers, digoxin, diuretics, prostaglandin infusion, and sildenafil.

  ii) Patients with PH are often taking warfarin, and they should be transitioned to low molecular weight heparin prior to their surgery.

    g) PH medications should be continued and doses should not be missed on the day of surgery.

    h) A complete blood count, metabolic panel, and coagulation panel should be evaluated. Consider preoperative blood gas analysis.

  i) An ECG should be performed to evaluate signs of ischemia or right-sided ventricular strain.

5) Anesthetic management

    a) Type of anesthetic

  i) Regional anesthesia is likely the best approach for PH patients if possible (peripheral nerve block or epidural but not spinal anesthesia), although data is limited and retrospective in nature.

  ii) Martin et al. showed that operative mortality in patients with Eisenmenger syndrome was 18% with general anesthesia versus 5% with regional anesthesia (6).

  iii) Conversely, Weiss et al. conducted a review of obstetric outcomes over 18 years, demonstrating similar outcomes using either general or regional anesthesia (7).

  iv) For moderate to severe PH, spinal anesthesia is contraindicated due to chance for abrupt alterations in SVR and preload.

    b) Maintain preoperative medications and continue the prostaglandin infusion, as even brief infusion interruptions can cause rapid deterioration and death.

  i) For patients taking sildenafil, avoid nitroglycerin and nitroprusside, which can cause severe hypotension.

  ii) Outpatient therapy is typically titrated slowly and carefully, so it is critical that this is not disrupted for elective surgery.

    c) Monitoring

  i) Arterial lines are indicated for all but the lowest risk surgeries.

  ii) Central venous access

(1) Caution should be taken during placement to avoid inducing arrhythmias.

(2) If atrial arrhythmias develop, cardioversion will avoid the rapid cardiovascular collapse that can occur.

  iii) Pulmonary artery catheters (PAC)

(1) The information gained by this monitor may provide critical information for ventilatory and inotropic management, making it recommended for most intermediate and all high-risk procedures.

(2) Caution must be used when inserting a PAC, which may be more difficult to place in a PH patient.

(3) PAC should not be placed in patients with Eisenmenger physiology (4).

  iv) TEE should be considered if available.

Table 62-1
Anesthetic and Hemodynamic Goals for patients with PH

    d) General anesthesia

  i) Sedation

(1) Supplemental oxygen should be used and preoperative sedation minimized to avoid hypoxia and hypercarbia.

  ii) Induction

(1) Anesthetic induction can be challenging due to the high resting sympathetic tone and resultant deficiency of catecholamine levels (5).

(2) This can result in exaggerated hemodynamic compromise following induction and as such, induction should be titrated slowly to effect.

(3) Induction are be carried out using a slow titration of narcotics, followed by an induction agent such as etomidate (0.2 to 0.4 mg/kg) to limit hemodynamic changes. Lidocaine (1 mg/kg) may also help blunt response to intubation and should be considered.

  iii) Maintenance of anesthesia

(1) Combinations of inhaled agents along with IV narcotics/benzodiazepines should be titrated to effect.

  iv) Fluid management

(1) Attempt to maintain euvolemia as close to baseline as possible.

(2) TEE/PAC measurements should guide fluid management with care taken not to overwhelm the RV function.

    e) Hemodynamic management

  i) If hypotension is observed, determine if it is due to RV failure or inadequate preload.

  ii) Assuming euvolemia, inotropic therapy must be considered. (Table 62-2)

  iii) Consider dobutamine (β₁ agonist) or milrinone (PDE III inhibitor) as IV inotropic therapy.

(1) Both agents are considered “inodilators” and may result in systemic vasodilation and hypotension, which can usually be treated with phenylephrine or norepinephrine.

  iv) Inhaled NO

(1) A potent pulmonary vasodilator (starting dose 20 to 40 ppm), which has minimal effect on systemic circulation (8).

(2) NO requires special equipment to administer inline in the anesthesia circuit, and not all hospitals have NO available.

(3) NO must be weaned slowly, so once started the patient will need to remain intubated as NO is weaned in the ICU.

(4) Inhaled prostacyclin has also been used intraoperatively either as continuous inhalational therapy (50 ng/kg/min) (9) or as an hourly inhaled bolus (50 μg over 15 minutes) (10).

  v) Vasoconstrictors such as phenylephrine, norepinephrine, and vasopressin may have variable responses on PVR, but may be needed in the setting of persistent systemic hypotension.

    f) Ventilator management

  i) Avoidance of hypoxia and hypercarbia is critical, but must be balanced by avoidance of lung hyperinflation.

  ii) Large alterations in lung volumes by positive pressure ventilation, along with either excessive or inadequate PEEP, can dramatically alter PVR in PH patients (5).

  iii) Low Tidal Volume Ventilation with low PEEP levels may be the ideal strategy, adjusting respiratory rate to prevent hypercarbia. Hypercarbia dramatically elevates PVR, and is a risk with this ventilation strategy and must be monitored carefully.

6) Postoperative management

    a) The postoperative period is a high risk time for PH patients.

    b) PH patients should be monitored in an intensive care setting in the first few days following surgery as there is high risk for sudden death.

    c) Patients may benefit from epidural anesthesia for postoperative analgesia.

    d) Finally, the patients should be transitioned back to their usual oral anticoagulation postoperatively.

References

1. Blaise G, Langleben D, Hubert B. Pulmonary arterial hypertension: pathophysiology and anesthetic approach. Anesthesiology 2003;99: 1415–1432.

2. Weitzel N, Gravlee G. Cardiac disease in the obstetric patient. In: Bucklin B, Gambling D, Wlody D, eds. A Practical Approach to Obstetric Anesthesia. 1st ed. Philidelphia, PA: Lippincott Williams & Wilkins; 2009:403–434.

3. McLaughlin VV, Archer SL, Badesch DB, et al. ACCF/AHA 2009 expert consensus document on pulmonary hypertension: a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents and the American Heart Association: developed in collaboration with the American College of Chest Physicians, American Thoracic Society, Inc., and the Pulmonary Hypertension Association. Circulation 2009;119:2250–2294.

4. Ray P, Murphy G, Shutt L. Recognition and management of maternal cardiac disease in pregnancy. Br J Anaesth 2004;93:428–439.

5. Huffmyer J, Rich G. Managing the patient with pulmonary hypertension who requires cardiac surgery. In: Cohen N ed. Medically Challenging Patients Undergoing Cardiothoracic Surgery. Philadelphia, PA: Lippincott Williams & Wilkins; 2009:185–214.

6. Martin JT, Tautz TJ, Antognini JF. Safety of regional anesthesia in Eisenmenger’s syndrome. Reg Anesth Pain Med 2002;27:509–513.

7. Weiss BM, Zemp L, Seifert B, et al. Outcome of pulmonary vascular disease in pregnancy: a systematic overview from 1978 through 1996. J Am Coll Cardiol 1998;31:1650–1657.

8. Sitbon O, Brenot F, Denjean A, et al. Inhaled nitric oxide as a screening vasodilator agent in primary pulmonary hypertension. A dose-response study and comparison with prostacyclin. Am J Respir Crit Care Med 1995;151:384–389.

9. Fiser SM, Cope JT, Kron IL, et al. Aerosolized prostacyclin (epoprostenol) as an alternative to inhaled nitric oxide for patients with reperfusion injury after lung transplantation. J Thorac Cardiovasc Surg 2001;121:981–982.

10. Hoeper MM, Schwarze M, Ehlerding S, et al. Long-term treatment of primary pulmonary hypertension with aerosolized iloprost, a prostacyclin analogue. N Engl J Med 2000;342:1866–1870.

Anesthesia for Aortic Surgery

James Sederberg, MD • Nathaen Weitzel, MD

1) Epidemiology and incidence of thoracic and abdominal aortic disease

    a) Definition and etiology

  i) An aneurysm is a permanent focal dilation of an artery to 1.5 times its normal size.

  ii) Aneurysms develop from the degradation of extracellular matrix proteins—elastin and collagen.

  iii) Smoking and infection may also play an important part by creating inflammation in the vessel wall (1).

    b) Surgical intervention is recommended based on overall aneurysm size, rate of expansion, patient age, and comorbidities. The annual risk of rupture is 3% in aneurysms 5 to 5.9 cm (2).

  i) Ascending thoracic aneurysm

(1) Surgery recommended for diameter >5.5 cm, or >6 cm in patients with increased operative risk. If patients are at increased risk of rupture or dissection, then repair is recommended at >5 cm (2).

  ii) Descending thoracic and abdominal aortic aneurysms (AAA)

(1) Intervention is recommended if aneurysm is >6 cm or growth rate >1 cm per year (3–5).

    c) Typical surgical and anesthetic complications

  i) Elective AAA repair has a mortality of < 2%, whereas rupture carries a mortality of up to 70% to 80% with 1% mortality per hour for the first 48 hours.

  ii) Complication rates are influenced by comorbid disease (Table 63-1) (6).

2) Physiology of aortic cross clamping

    a) Thoracic/supraceliac (Table 63-2)
Hemodynamic changes associated with proximal aortic occlusion include (10):

  i) Increased afterload, with an increase in proximal aortic pressure

  ii) Elevated LV wall tension with increased myocardial O₂ consumption

  iii) Increased preload due to decreased venous capacitance below the clamp. This results in volume redistribution from the splanchnic and nonsplanchnic beds toward the heart.

  iv) Severe hypertension (HTN) during aortic occlusion

(1) Often associated with clamping along with a reflexively decreased heart rate

(2) Increase in cardiac contractility secondary to cathecholamine release

(3) Treatment of HTN is often difficult while still maintaining spinal cord and distal perfusion pressures.

   (a) Nitroglycerin, sodium nitroprusside, esmolol, epidural infusions, high-dose narcotics, and increased anesthetic depth may be used to treat HTN during aortic occlusion.

    b) Abdominal/infraceliac ( Table 63-2)

  i) The same effects on afterload and contractility occur when the abdominal aorta is cross-clamped; however, effects on preload are inconsistent (8).

  ii) Preload has been observed to increase, likely secondary to the same mechanism as in a supraceliac clamp.

    c) Unclamping (Table 63-3)—As the cross-clamp is released, the opposite physiologic effects are seen with a marked decrease in systemic vascular resistance (SVR), central hypovolemia, and hypotension.

  i) This is caused by blood pooling in reperfused tissues, hypoxia-mediated vasodilation, and accumulation of myocardial depressant and vasodilatory metabolites such as lactate.

  ii) Left ventricular end-diastolic pressure decreases and myocardial blood flow increases (7,8).

  iii) The celiac and/or superior mesenteric arteries are often involved with suprarenal cross-clamp placement. This can produce visceral ischemia and profound lactic acidosis, therefore sodium bicarbonate, along with slow release of the cross clamp, is beneficial.

  iv) If severe unclamping shock occurs, replacement of the clamp will restore BP until further volume resuscitation can be accomplished.

1) Thoracic aortic aneurysms (TAAA)

    a) Descending thoracic aneurysms begin distal to the left subclavian artery and are classified using the Crawford classification (Fig. 63-1)

  i) Type I aneurysms originate below the left subclavian artery and extend to the celiac axis

  ii) Type II originate as Type I, but extend to the infrarenal aorta.

  iii) Any aneurysm involving the ascending aorta or arch is also considered a Type II aneurysm.

  iv) Type III begins in the distal thoracic aorta and involves the remainder of the abdominal aorta.

  v) Type IV begins at the diaphragm and involves the entire abdominal aorta.

    b) Anesthetic considerations

  i) Preoperative considerations

(1) Preanesthesia evaluation

   (a) Many patients are smokers with cardiac and/or pulmonary disease including HTN, coronary artery disease, Chronic Obstructive Pulmonary Disease (COPD), or bronchitis.

   (b) A thorough preoperative multisystem workup must be carried out with special focus on the cardiac and pulmonary systems.

     (i) Pulmonary Function Testing, chest radiograph, and cardiac stress testing are often indicated. Basic labs should also be obtained.

  ii) Intraoperative considerations

(1) Monitoring choices and considerations.

(2) Standard ASA monitors plus an arterial line is typically used.

(3) A right radial arterial line is preferred in case the cross clamp is applied proximal to the subclavian artery. An additional femoral arterial line may be useful depending on the surgical clamping strategy.

(4) Large bore peripheral IV and central venous access are essential.

(5) A pulmonary artery catheter (PAC) or transesophageal echocardiography (TEE) can give vital information about hemodynamic changes and volume status, and is indicated in patients with known cardiac disease (9).

(6) The patient should have a type and cross for four units of packed red blood cells.

(7) Vasoactive infusions and heparin should be readily available.

  iii) For induction, the choice of agent is not as critical as is the manner delivered.

(1) Induction should be achieved with careful and slow titration of narcotics, hypnotics, and muscle relaxants.

(2) The goal is to maintain hemodynamic stability while preventing overt HTN, and to blunt the sympathetic response to endotracheal intubation.

  iv) Airway management

(1) Lung isolation is usually necessary for Crawford type I, II, and some type III aneurysm repairs (3).

(2) Double lumen endotracheal tube is preferred over endobronchial blockers because of the increased ability to clear secretions and the ability to provide Positive End Expiratory Pressure (PEEP) to the dependent lung and/or Continuous Positive Airway Pressure (CPAP) to the nondependent lung.

  v) Surgical considerations

(1) A left-sided thoracotomy is the preferred approach with patients typically placed in a modified right lateral decubitus position. The exact location of the incision depends on the extent of aortic pathology.

    c) Specific perfusion scenarios

  i) Circulatory arrest

(1) The goals of deep hypothermic circulatory arrest (DHCA) are to protect the vital organs by reducing metabolic rate and to protect the brain and heart from re-warming.

(2) Temperatures are typically reduced to 10°C to 18°C, which allows a safe duration of approximately 40 minutes.

(3) Cooling and re-warming should be gradual, and a differential temperature gradient (esophageal-blood) of more than 10°C should be avoided.

(4) During DHCA, the head should be packed in ice (with care taken to avoid the eyes), which typically achieves isoelectricity on an electroencephalogram (EEG) or processed EEG monitor before arrest.

(5) Use of steroids, propofol, or barbiturates may be also helpful.

  ii) Anterograde cerebral perfusion (ACP)

(1) The goal is to maintain the brain temperature at selected levels, meet the demands of metabolism, and remove the cerebral metabolic waste during ischemia.

(2) The subclavian or innominate artery can be cannulated for this purpose, or to provide bihemispheric protection, the left common carotid artery as well.

(3) This is a low flow scenario using approximately 10 mL/kg/min flow rates (to achieve pressures near 40 mm Hg), coupled with hypothermia for protection. Studies demonstrate conflicting data regarding absolute length of time ACP can be safely carried out (9,10).

  iii) Partial bypass or left heart bypass (II) may be required during more extensive aortic repairs. Oxygenation can be through the lungs or an oxygenator.

    d) Anti-coagulation considerations

  i) Coagulopathy

(1) Platelet dysfunction and coagulopathy are often seen following prolonged cardiopulmonary bypass and DHCA.

(2) Coagulation studies can help guide transfusion decisions, and thromboelastography can be invaluable.

    e) Spinal cord protection/neurologic protection

  i) Neurological injury is a devastating consequence of aneurysm repair, especially thoracic aorta aneurysm repair.

  ii) Risks include emergency surgery, dissection, extensive disease, prolonged cross clamp time, rupture, level of clamp, age, and history of renal dysfunction.

  iii) Cerebrospinal fluid (CSF) drain

(1) Aortic cross-clamping causes elevation of CSF pressure.

(2) The spinal cord perfusion pressure (SCCP) is the difference between spinal arterial pressure and CSF pressure. ↓CSF pressure → improved SCCP.

(3) Goals are to keep spinal drain pressure around 10 mm Hg, and drainage should be limited to a maximum of 20 mL/h.

  iv) Spinal cord blood flow

(1) The spinal cord is perfused by two posterior arteries, which supply approximately 25% of the spinal cord and one anterior artery that supplies 75% of the spinal cord.

(2) The most important radicular artery is the artery of Adamkiewicz, which arises from T9 to T12 in 60% of people, and supplies the anterior spinal artery of the upper thoracic spinal cord. If this artery comes from the aneurysm wall or below the cross-clamp, then spinal cord ischemia and anterior spinal artery syndrome are possible.

  v) Electrophysiologic monitoring of spinal cord

(1) Monitoring of evoked potentials provides the surgeon with opportunity to promptly intervene if the monitoring shows potential neurological compromise. A decrease in amplitude or an increase in latency can be indicative of pathway interruption.

(2) Somatosensory evoked potentials (SSEPs) monitor the integrity of the posterior sensory pathway, the posterior and lateral column of the spinal cord.

(3) Motor evoked potentials (MEPs) stimulate the motor cortex and record at the level of the spinal cord, peripheral nerves, or muscles and monitor the vulnerable anterior portion of the spinal cord.

(4) Monitoring SSEPs and MEPs are often used in conjunction in TAAA surgery (7).

    f) Renal protection and fluid management

  i) Renal failure is a common occurrence in aortic surgery and carries a high risk of mortality. There have been multiple techniques used to protect the kidneys including

  ii) Low-dose dopamine

(1) Dopamine has α, β, and DA2 as well as DA1 receptor effects (which may actually limit renal blood flow, GFR, and sodium excretion and thus contributing to renal injury). Current evidence indicates no benefit associated with the use of dopamine for renal protection (12).

  iii) Fenoldopam

(1) DA-1 specific agonist with systemic vasodilator properties has been used to help protect the kidneys.

(2) Used at low doses (0.05 to 1.0 μg/kg/min), it has been shown to increase urine output and decrease renal replacement therapy and all cause mortality (13).

(3) Should be continued into the perioperative period for at least 48 hours.

  iv) Mannitol

(1) Often given as well to help improve renal blood flow and protect the kidneys.

  v) Fluid therapy

(1) Replace fluid and blood loss aggressively to maintain renal perfusion.

(2) The goal is to keep renal perfusion adequate and to maintain a urine output of ≥0.5 mL/kg/h (13,14).

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