I. INTRODUCTION
II. OVERVIEW OF HEART FAILURE (HF)
III. PATHOPHYSIOLOGY OF HEART FAILURE
Overview
HF may be described in terms of the ventricle that is initially impaired.
Fluid accumulates behind (upstream to) the affected chamber.
TABLE 9-1 Clinical Findings in Heart Failure
Left-Sided Heart Failure
Right-Sided Heart Failure
Systolic
Diastolic
Anxiety
Sudden light-headedness
Fatigue, weakness, lethargy
Orthopnea
Dyspnea, dyspnea on exertion
Paroxysmal nocturnal dyspnea
Tachypnea (on exertion)
Cheyne-Stokes respirations (if severe)
Diaphoresis
Palpitations
Sacral edema, pitting of extremities
Basilar rales, rhonchi, crackles, wheezes
Cool, moist, cyanotic skin
Hypoxia
Respiratory acidosis: ↑ pH and ↑ PaCO2
↑ pulmonary artery diastolic pressure
↑ pulmonary capillary wedge pressure
Nocturia
Mental confusion
↓ pulse pressure
Pulsus alternans
Lateral displacement of point of maximal impulse
S3, S4 heart sounds
Murmur of mitral insufficiency
Exercise intolerance
Orthopnea
Dyspnea, dyspnea on exertion
Paroxysmal nocturnal dyspnea
Cough with frothy white or pink sputum (in pulmonary edema)
Tachypnea (on exertion)
Basilar crackles, rhonchi, wheezes
CXR: pulmonary edema
Hypoxia
Respiratory acidosis: ↑ pH and ↑ PaCO2
↑ pulmonary artery diastolic pressure
↑ pulmonary capillary wedge pressure
S3, S4 heart sounds
Holosystolic murmur (if tricuspid, mitral regurgitation)
Symptoms of right-sided heart failure
Dependent pitting edema
Fatigue, weakness
↓ exercise tolerance
Weight gain or loss
Anorexia
Ascites
Cachexia
Nausea, vomiting
Abdominal pain (from liver congestion)
Hepatomegaly
Hepatojugular reflux
Venous distention
Splenomegaly
Hypotension
Bounding pulses
S3, S4 heart sounds
Murmur of tricuspid insufficiency
↑ CVP, RA, and RV pressures
CXR: enlarged RA, RV
Dysrhythmias
Oliguria
Nocturia (secondary to ↑ renal
perfusion when patient is lying in bed)
Kussmaul’s sign (constrictive cardiomyopathy):
paradoxical ↑ in venous distention and pressure during inspiration
CXR, chest x-ray; CVP, central venous pressure; PaCO2, arterial partial pressure of carbon dioxide; RA, right atrium; RV, right ventricle. Adapted from Lessig ML. The cardiovascular system. In: Alspach JG, ed. Core Curriculum for Critical Care Nursing. 6th ed. Philadelphia, PA: Elsevier; 2006:185-380; Garg A, Vignesh C, Singh V, Ray S. Acute right heart syndrome: rescue treatment with inhaled nitric oxide. Indian J Crit Care Med. 2014;18(1):40-42; Jaski B. The 4 Stages of Heart Failure. Minneapolis, MN: Cardiotext Publishing, 2015:6-8, 21-31, 86-95, 103-110.
LV failure: Fluid accumulates in the pulmonary capillary bed.
RV failure: Fluid accumulates in the systemic venous circulation.
Overview
HF can also be characterized by abnormalities in systolic and/or diastolic function—based on whether the dysfunction stems from an inability of the ventricle to contract normally and pump sufficient blood (systolic HF) or an inability of the heart to relax and fill normally (diastolic HF).
Heart failure with preserved ejection fraction (HFpEF) is a form of diastolic dysfunction. Heart failure with reduced ejection fraction (HFrEF) is characterized by systolic dysfunction.5
TABLE 9-2 Etiology of Heart Failure
Cardiomyopathy
Infection
Metabolic Disorders
Electrolyte Deficiency
Nutritional Disorders
Systemic Diseases
Toxins
Dilated (idiopathic)
Hypertrophic
Restrictive
Ischemic
Valvular:
Chagas’ disease Infection
Endocrine:
Diabetes mellitus
Thyroid disease
Adrenal insufficiency
Pheochromocytoma
Acromegaly
Familial storage disease:
Hemochromatosis
Glycogen storage disease
Hypokalemia
Hypomagnesemia
Kwashiorkor anemia
Thiamine deficiency (beriberi)
Selenium deficiency
Carnitine deficiency
Connective tissue disorders
Systemic lupus erythematosus
Scleroderma
Sarcoidosis
Rheumatoid arthritis
Polyarteritis nodosa
Polymyositis
Connective tissue disorders
Systemic lupus erythematosus
Scleroderma
Sarcoidosis
Rheumatoid arthritis
Polyarteritis nodosa
Polymyositis
Amyloidosis
Alcohol
Cocaine
Radiation therapy
Chemotherapeutic agents (e.g., anthracyclines)
Chemicals (e.g., hydrocarbons, lead)
Viral
Bacterial
Fungal
Obstruction
Insufficiency
Hypertensive
Infective (viral)
Peripartum
Familial
From Kallikazaros I. Heart failure with preserved ejection fraction. Hellenic J Cardiol. 2014;55:265-266; Komamura K. Review article. Similarities and differences between the pathogenesis and pathophysiology of diastolic and systolic heart failure. Cardiol Res Pract. 2013;2013:Article ID 824135; Blair J, Huffman M, Shah S. Heart failure in North America. Curr Cardiol Rev. 2013;9:128-146.
HFpEF or diastolic dysfunction5
A patient with HFpEF will usually have one or more disease processes: diastolic dysfunction from the impaired LV relaxation and/or increased LV diastolic stiffness, enlarged LV size, increased LV volume, increased arterial and ventricular stiffness, and abnormal systolic function.6
Diagnosis of this clinical syndrome requires that these three criteria be fulfilled:
Signs and symptoms of HF
EF > 45%
Evidence of diastolic dysfunction echocardiographically or hemodynamically or equivalent (concentric left ventricular hypertrophy, increased LV size, atrial fibrillation, or elevated brain natriuretic peptide [BNP] levels).6
Restrictive cardiomyopathy, hypertrophic cardiomyopathy, constrictive pericarditis, and valvular cardiomyopathy are common diagnoses/disease pathologies in the majority of patients with HFpEF (Table 9-2).
Restrictive (the heart is stiff and unable to relax correctly); this can be caused by
Radiation therapy causing scarring to the heart.
Amyloidosis causes abnormal protein fibers to accumulate in the heart muscle.
Sarcoidosis produces lumps (called granulomas) in the heart and other organs.
Hemochromatosis is a genetic condition that causes iron to build up in the heart and other parts of the body.
Post-heart transplant restrictive cardiomyopathy is associated with the development of diffuse small vessel transplant coronary artery disease.
Hypertrophic (enlarged heart)—ventricular walls get thicker and the heart chamber becomes smaller, thereby limiting the filling and pumping ability. It may be congenital (hypertrophic cardiomyopathy) or acquired (e.g., hypertensive heart disease, aortic stenosis).
Valvular (caused by structural defects to the heart valves altering flow within the heart and circulation. Can lead to enlarged chambers and decreased function).
Defined as pulmonary or systemic venous congestion in the setting of near normal systolic function
Hemodynamically, the principal abnormality of diastolic failure is the inability of the ventricles to relax and fill adequately. This leads to elevated left ventricular end-diastolic pressure (LVEDP) and may be associated with
Systemic hypertension
S4 gallop
Normal or increased EF
Small LV cavity, concentric LV hypertrophy
HFrEF or systolic dysfunction7
HF can occur with reduced ejection fraction (HFrEF) as defined by an EF < 40% or systolic HF.8 The patient with HFrEF may have a low cardiac output (CO) state whereby the LV cannot pump oxygen-rich blood to the systemic circulation. The weakened LV remodels and dilates, thereby enlarging the chamber, increasing LV volume and pressure. This further weakens the LV and may dilate the mitral valve annulus leading to a backup of blood (functional mitral regurgitation).
Left atrial (LA) pressure and volume increase when blood inadequately empties into the LV. This volume backs up into the lungs via the pulmonary venous system. As pulmonary pressures increase (pulmonary hypertension) and pulmonary capillary wedge pressure (PCWP) exceeds 24 mm Hg (oncotic pressure), the ensuing pulmonary congestion symptomatically causes an increased work of breathing, dyspnea, cough, pleural effusions, and respiratory failure if left untreated.7,8
Nonischemic, idiopathic, viral, ischemic, familial, valvular, and postpartum are common cardiomyopathy diagnoses/disease pathologies in the majority of patients with HFrEF (see Table 9-2).
Ischemic (caused by loss of blood supply to the heart, typically related to coronary artery disease)
Nonischemic—heart failure with reduced EF, with normal coronaries. Variety of possible causes are listed below:
Idiopathic (unknown cause)
Viral (bacterial or viral infections can inflame and damage the heart muscle [myocarditis])
Familial: Inherited genes in the family that may be responsible for the cardiomyopathy
Valvular (caused by structural defects to the heart valves altering flow within the heart and circulation. Can lead to enlarged chambers and decreased function)
Postpartum (can occur during last trimester or within 6 months after pregnancy)
Congenital: born with a structural heart defect
Alcohol (resulting from chronic alcohol use)
Drug abuse (causing irreversible damage to the heart, e.g., cocaine, methamphetamines)
Other causes of HFrEF include the following:
Long-standing uncontrolled hypertension
Tachycardia-related cardiomyopathy
Hyperthyroidism
Advanced infiltrative diseases (sarcoid, amyloid, hemochromatosis)
Hypertrophic cardiomyopathy9
Impaired myocardial contractility leads to weakened systolic contraction.
Hemodynamically, HFrEF is associated with
Normal or low blood pressure (BP).
S3 gallop.
Decreased CO.
Reduced stroke volume (SV).
Increased ventricular diastolic pressure.
Decreased EF: the amount of blood ejected in a single heartbeat relative to the total LV volume; normal EF is approximately 60%.
Large, dilated heart on chest radiograph.
May be caused by a primary RV injury/abnormality or increased pressure in the pulmonary vasculature leading to elevated right heart pressure and eventually failure.
The RV is not able to pump blood into the pulmonary system.
As the RV fails, there is systemic venous congestion and hypoperfusion.
LV failure is the most common cause of RV failure.
LV failure typically precedes RV failure except in the setting of
RV infarct
Arrhythmogenic RV dysplasia
Certain primary pulmonary disease processes (chronic pulmonary arterial hypertension, acute respiratory distress syndrome [ARDS], or pulmonary emboli [PE])
IV. EVALUATION OF OBJECTIVE MEASURES OF END-STAGE HEART DISEASE: POTENTIAL FINDINGS
Heart rate (HR)
May be increased in an attempt to maintain CO
With systolic and diastolic dysfunction, stroke volume (SV) is decreased; this may precipitate a compensatory increase in HR (CO = SV × HR).
May be decreased due to effects of β-blockers or ivabradine (Corlanor)
Heart rhythm
May be irregular due to atrial fibrillation, atrial flutter, or supraventricular tachycardia with variable atrioventricular block.
Pulsus alternans: Pulse has normal rate, but you can feel (or see on an arterial line tracing) strong beats alternating with weak beats. This is associated with an alternating impairment in LV preload.
Blood pressure
Assess for hypotension and hypertension.
Typically maintained as low as tolerable (without causing symptoms such as light-headedness or dizziness), so as to decrease myocardial workload.
May be low in right-sided HF.
Weight
Think of weight as an HF vital sign.
Always check daily weights in the hospital and ask the patient to continue daily weights at home and report this information to the doctor upon every encounter.
Weigh patients in the morning using the same scale and technique for accuracy.
On admission, check height and weight and calculate a body mass index (BMI). A BMI > 30 has been correlated with poor transplant outcomes and is a relative contraindication to transplantation.10
Fluid balance
Carefully record and monitor all daily fluid input and output. HF patients typically require fluid restriction (<1.5 L/day).
Heart failure lethal triad4
Hypotension (systolic BP < 100).
Activation of sympathetic nervous system (indicated by heart rate [HR] > 100).
Activation of renin-angiotensin system (indicated by serum sodium [Na+] < 130). Hyponatremia can be due to volume overload or sodium depletion from diuretic use.
TABLE 9-3 Heart Failure: Potential Abnormal Findings | ||||||||||||||||||||||||||||||||||
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Head exam:
Assess temples for temporal wasting (look for a pronounced indentation in the appearance of the muscles covering the temporal bones). This is present in cases of advanced HF and is a sign of malnutrition.
Look at the sclera for jaundice indicating liver disease from passive congestion, hepatitis, or possibly cirrhosis.
Neck veins:
Place the patient at a 30-degree incline. Jugular venous pressure (JVP) is estimated by placing a ruler on the patient’s sternum at the level of the second intercostal space (angle of Louis).
Turn the patient’s head to the side to better visualize the neck veins.
Measure to the top of the visible distended internal jugular neck vein and add 5 cm.
If there are no visible neck veins, take your other hand and compress the middle of the abdomen. If the neck vein now distends and remains elevated, the patient has a positive abdominal jugular reflex (AJR). This is a positive sign for fluid volume overload even though the neck veins appeared normal.
Heart sounds:
A third heart sound (S3) or ventricular gallop results from a reduced EF and impaired diastolic function.
A fourth heart sound (S4) or atrial gallop reflects a lack of ventricular compliance due to ischemic heart disease, hypertension, or hypertrophy.
Pulmonary assessment:
Pulmonary crackles can be auscultated if fluid is leaking from the capillaries into the alveolar spaces. Over time, crackles increase and effusions can develop. However, patients with chronic HF may not have crackles.
Pulmonary hypertension is assessed with pulmonary artery catheter monitoring.
Gastrointestinal (GI) assessment:
Review liver function and viral hepatitis tests.
Palpate liver for enlargement.
Skin and hair assessment: The condition of the skin and hair will reveal the state of the HF, perfusion, oxygenation, and nutrition. It can also unveil underlying diseases such as thyroid disorders, diabetes, neuropathies, and vascular disorders.
Color (cyanosis, jaundice, hyperpigmentation)
Cyanosis is a bluish color in the skin that can indicate reduced CO, peripheral vascular disease, or anemia.
Jaundice is a yellowing of the skin that can indicate passive liver congestion secondary to heart failure or underlying liver disease.
Hyperpigmentation (skin that has changed from normal to bronze) can result from sun damage, inflammation, or a variety of diseases. Excess iron or hemochromatosis should be considered.
Temperature: Cool, lower extremities with delayed capillary refill may indicate a low CO or PVD.
Moisture: Clammy, moist skin can be related to hypoperfusion, low cardiac output state.
TABLE 9-4 STOP-BANG© Questionnaire
This yes/no questionnaire is used to assess if the patient has potential for obstructive sleep apnea (OSA).
Do you Snore Loudly (loud enough to be heard through closed doors or loud enough that your bed partner wakes you)?
Yes
or
No
Do you often feel Tired, Fatigued, or Sleepy during the daytime (do you fall asleep during usual activities, work, driving, etc.)?
Yes
or
No
Has anyone Observed you Stop Breathing, Choking, or Gasping during your sleep?
Yes
or
No
Do you have or are you being treated for High Blood Pressure?
Yes
or
No
Is your Body Mass Index more than 35 kg/m2
Yes
or
No
Are you age 50 or older?
Yes
or
No
Do you have a large neck size? (measured around Adam’s apple)
For male, is your shirt collar 17 inches/43 cm or larger?
For female, is your shirt collar 16 inches/41 cm or larger?
Yes
or
No
Are you a Male?
Yes
or
No
Scoring the STOP-BANG for the general population
OSA—low risk: yes to 0 to 2 questions
OSA—intermediate risk: yes to 3 to 4 questions
OSA—high risk: yes to 5 to 8 questions
or yes to 2 or more of 4 STOP questions + male gender
or yes to 2 or more of 4 STOP questions + BMI > 35 kg/m2
or yes to 2 or more of 4 STOP questions + neck circumference 17 inches/43 cm in male or 16 inches/41 cm in female
Adapted from the STOP-BANG Questionnaire and reprinted with the permission of the Toronto Western Hospital University Health Network.
From Luo J, Huang R, et al. Value of STOP-BANG questionnaire in screening patients with obstructive sleep hypopnea syndrome in sleep disordered breathing clinic. Chin Med J (Engl). 2014;127(10):1843-1848; Mehra R. Sleep apnea ABCs: airway, breathing, circulation. Cleve Clin J Med. 2014;81(8):479-489.
Edema or swelling in the legs, abdomen, or areas around the eyes.
Hair thinning
Hair follicles survive by the blood flowing through veins and arteries; when this is reduced, hair loss can occur.
Hairless legs, feet, or toes are a red flag for malnutrition and thyroid or vascular disease, which can lead to stroke and myocardial infarction.
Chest radiograph may be normal in some patients.
Abnormal chest radiograph findings may include the following:
Pulmonary vasculature: Pulmonary edema or congestion associated with left-sided HF.
Cardiac silhouette: Heart may be enlarged.
Enlarged right atrium (RA) or RV: Indicative of right-sided HF.
Pleural effusions: May be associated with left-sided failure.
Valve calcifications: May be associated with valvular disease.
Placement of any lines and pacemakers or indications of past cardiac surgeries, such as sternal wires.
Presence of any coexisting mediastinal, thoracic, or pulmonary diseases, nodules, or tumors.
May indicate nonspecific changes
LV hypertrophy
Q waves from old myocardial infarction (MI)
Atrial dysrhythmias and bundle-branch blocks common.
High incidence (70% to 80%) of atrial fibrillation.6
Atrial fibrillation often is secondary to LA enlargement.
Dysrhythmias may be associated with ischemic heart disease, conduction abnormalities, electrolyte imbalances, and other factors.
Increased QRS voltage may indicate LV enlargement.
QRS duration > 120 ms and left bundle-branch block (LBBB) morphology may indicate need for biventricular pacing.
The echocardiogram allows the cardiologist to visualize all valves and chambers of the heart, estimate right and left heart filling pressure, and assess systolic and diastolic function to more accurately diagnose the specific type of cardiomyopathy. Different cardiomyopathies will have distinguishing features reflected in the appearance of the ventricular wall chamber size, thickness, and function.
Chamber size:
Dilated cardiomyopathy: As myocardial fibers degenerate and become fibrotic, atria and ventricles dilate.
The etiology of the damaged myocardium may be due to the following etiologies: Idiopathic, viral, ischemic, toxic (alcohol, drugs), pregnancy, genetic, myocarditis (human immunodeficiency virus [HIV] infection, Chagas’ disease), chemotherapy, or stress (Takotsubo).
Wall thickness:
LV dilatation and hypertrophy are common in hypertrophic cardiomyopathy.
Ejection fraction (EF):
Left ventricular EF varies depending on the pathology and is not used as criteria for transplantation; it is used to assess decompensation and treatment response.10
Thrombus formation:
Atrial fibrillation: Potential for thrombi formation in atria (requires anticoagulation therapy); typically detected by transesophageal echocardiography
LV hypokinesis, systolic dysfunction, and aneurysm: Potential for thrombi formation in the LV due to stasis of blood flow contributing to clot formation
If thrombus is noted, anticoagulation is required.
Valve function:
Dilatation of mitral annulus may occur secondary to LV dilatation.
Primary valvular disease may be the cause of cardiomyopathy.
Systolic and diastolic function:
Diastolic function can be measured by echocardiography using a number of parameters including color flow Doppler, myocardial strain, and tissue Doppler.
Pericardial effusion: Abnormal amount of fluid collecting inside the heart sac located between the heart and pericardium
Pericardial effusions: Potential etiologies include, but are not limited to,
Infection
Myocardial infarction
Injury to the pericardium during a surgery or medical procedure
Uremia
Autoimmune diseases (lupus, rheumatoid arthritis)
Large pericardial effusions can result in cardiac tamponade (hypotension, JVD, and muffled heart sounds), which is a medical emergency.
Right heart catheterization:
To assess right heart pressures and volume status: See “Clinical Findings in Left-Sided and Right-Sided Heart Failure.”
To assess CO and perfusion state in patients who may require inotropic support.
To assess PVR and transpulmonary gradient.
If the PVR > 5 woods unit or the TPG >15 are irreversible, the patient may not be a candidate for heart transplantation.10
To perform endomyocardial biopsy (EMB) if myocarditis or an infiltrative disease process is suspected and diagnosis will guide treatment.
Left heart catheterization:
Assess coronary artery anatomy and determine potential for coronary revascularization.
Measure left ventricular pressures.
Determine ventricular size and contractility (i.e., EF).
Evaluate valve function.
Detect structural defects.
To diagnose and treat supraventricular and ventricular arrhythmias
VO2 max is a measurement of oxygen consumption at peak exercise.
The failing heart does not have the ability to provide sufficient oxygen to meet the aerobic needs of the peripheral tissues, thus increasing CO2 and lactic acid production during anaerobic metabolism.
An VO2 max <14 mL/kg/min or <50% predicted for age is typically used to determine transplant candidacy.10
TABLE 9-5 Laboratory Tests | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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TABLE 9-6 New York Heart Association Classification of Heart Failure | ||||||||||||||
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TABLE 9-7 Heart Failure Progression | ||||||||||||||||||||||||||||
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 FIGURE 9-1 Stages in the evolution of HF and recommended therapy by stage. |
V. TREATMENT OF HEART FAILURE
Hypertension and lipid disorders should be controlled to lower HF risk (level of evidence A [Table 9-8]).18,20
HF education to facilitate self-care should include symptom monitoring, daily weights, heart-healthy diet low in sodium, fluid restriction, safe medication practices, and routine physical exercise to increase exercise tolerance (level of evidence B).
Cardiac rehabilitation may reduce mortality and hospitalization and improves functional capacity, exercise duration, and quality of life (level of evidence B).
Treatment of sleep disorders with continuous positive airway pressure can increase left ventricular ejection fraction (LVEF) and functional status in patients with HF and sleep apnea (level of evidence B).
Other conditions that may contribute to HF, such as obesity, diabetes mellitus (DM), tobacco use, and any cardiotoxic drug abuse (cocaine, methamphetamines), should be avoided or controlled (level of evidence C).
Sodium restriction (e.g., ≤2 g/day) is recommended for HF patients to prevent fluid accumulation or facilitate diuresis (level of evidence C).
Fluid restriction (e.g., ≤ 2 L/day) to help prevent fluid accumulation.
The American Heart Association (Get with the Guidelines) recommends the following for treatment as a standard of care for patients with LVEF≤ 40%, unless contraindicated:
Angiotensin-converting enzyme inhibitors (ACE)/angiotensin II receptor blockers (ARB)
Beta-blockers
Aldosterone antagonists
Hydralazine/nitrates (for African Americans with LV dysfunction)
ICD if EF is <35%; or cardiac resynchronization therapy-defibrillation (CRT-D) device therapy is indicated when the EF < 35% and the QRS duration is 120 ms or greater with LBBB.
The following beta-blockers, bisoprolol (Zebeta), carvedilol (Coreg), and metoprolol succinate (Toprol-XL), but not metoprolol tartrate (Lopressor), have evidence to show reduced morbidity and mortality in patients with systolic HF.
↑ dyspnea at rest or with exertion
↑ orthopnea
↑ paroxysmal nocturnal dyspnea
↑ weakness, fatigue
↓ appetite and/or early satiety
↑ abdominal fullness
Difficulty sleeping
Development of chest pain/pressure or ↑ in angina
↑ edema (abdominal, peripheral)
New-onset or worsening dysrhythmias
Weight gain >3 lb for more than 2 consecutive days
Vomiting
Development of cardiac cachexia
New onset or increasing frequency of syncope
↑ serum creatinine >2.0 mg/dL (may be secondary to use of diuretics and ACE inhibitors)
↑ blood urea nitrogen >50 mg/dL (unless patient has intrinsic renal disease)
Serum sodium <134 mEq/L
↑ liver enzymes and bilirubin over baseline
Diuretic unresponsiveness
↑ brain natriuretic peptide level over baseline level in certain patients
TABLE 9-8 Medical Evidence Scale | ||||||||||||||||||||||
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VI. HEART TRANSPLANTATION
First heart transplant: December 3, 1967, Cape Town, South Africa, by Dr. Christiaan Barnard23
Confirmed that heart transplantation was technically possible and that a transplanted heart could indeed sustain life.
This early success gave rise to the worldwide development of heart transplant centers in the late 1960s and early 1970s. However, without effective immunosuppression, heart transplantation outcomes were poor, and therefore, heart transplantation was not deemed a viable therapeutic option.
In the 1970s, two important advances revolutionized the field of heart transplantation: The development of the EMB procedure24 and the discovery of cyclosporine.25,26 These advances improved survival, and since 2000, approximately 3,000 heart transplant procedures per year have been reported to the International Society for Heart and Lung Transplantation (ISHLT).
Terminal HF that is unresponsive to optimal medical therapy
Refractory HF requiring inotropic or MCS with reversible end-organ damage
Refractory angina, not amenable to revascularization, on optimal medical therapy
TABLE 9-9 Pharmacologic Therapy for Heart Failure
Medication
Action(s)
Diuretics
↓ intravascular and extravascular fluid volume, thereby ↓ preload
Angiotensin-converting enzyme (ACE) inhibitors
↓ afterload by blocking the formation of angiotensin II and inhibiting the release of aldosterone, thereby ↓ sodium retention
↓ preload via vasodilation
Angiotensin II receptor blockers (ARBs)
↓ blood pressure by blocking the vasoconstrictor and aldosterone-secreting effects of angiotensin II
β-Adrenergic receptor antagonists (β-blockers)
↓ preload
Aldosterone antagonists (spironolactone)
↓ preload by ↑ excretion of sodium and water
Direct-acting vasodilators (hydralazine/nitrates)
↓ preload
Nitrates
↓ preload via dilatation of systemic veins and by ↓ venous return, thereby ↓ LV filling pressure
↓ afterload by vasodilation of systemic arteries
Anticoagulants
↓ risk of thromboembolism associated with atrial fibrillation, LV hypokinesis, or systolic dysfunction
Digitalis glycosides
↓ preload
May be used for rate control in setting of atrial fibrillation or atrial flutter
Inotropic agents: milrinone
↑ myocardial contractility without ↑ heart rate
↓ afterload and preload via arterial and venous smooth muscle relaxation and by ↑ peripheral vasodilation
Inotropic agents: dobutamine
↑ myocardial contractility
↑ stroke volume and cardiac output
↓ systemic vascular resistance
Nesiritide (human B-type natriuretic peptide)
↑ vasodilation, ↓ pulmonary capillary wedge pressure, ↑ renal blood flow, and ↑ urinary output
Vasopressors: dopamine
Dose: 2-10 mcg/kg/min (β-adrenergic effects): ↑ vasoconstriction, ↑ blood pressure, and ↑ renal and cerebral perfusion
Dose: > 10 mcg/kg/min: α-adrenergic effects: peripheral vasoconstriction; ↑ systemic vascular resistance, ↑ afterload and blood pressure; may possibly ↓ cardiac output
Vasopressors: phenylephrine hydrochloride
↑ blood pressure via arteriolar vasoconstriction;↑ stroke volume; may ↓ heart rate
Starling R. Medical grand rounds advanced heart failure transplant, LVADs, and beyond. Cleve Clin J Med. 2013;80(1):33-40; Fang KC, Ewald GA, Allen LA, et al. Advanced (stage d) heart failure: a statement from the heart failure society of America guidelines committee. J Card Fail. 2015;21(6):519-534; Reed BN, Rodgers JE, Sueta, CA. Polypharmacy in heart failure: drugs to use and avoid. Heart Fail Clin. 2014;10(4):577-590; Yancy CW, Jessup M, et al. 2013 ACCF/AHA Guideline for the Management of Heart Failure: a Report of the American College of Cardiology Foundation/American Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;62(16):147-239.
Refractory, life-threatening dysrhythmias
Congenital heart disease with progressive ventricular failure not amenable to conventional surgical repair
Any NYHA Class 4 HF where the transplant selection team deems that the cardiomyopathy is associated with a poor short-term prognosis without transplantation
FIGURE 9-2 Mechanical circulatory support.
Types of cardiomyopathies leading to heart transplant may include the following:
Ischemic, nonischemic, idiopathic, viral, valvular, restrictive, postpartum, familial, congenital, hypertrophic, and arrhythmogenic right ventricular dysplasia (ARVD)
Severity of the patient’s functional impairment
Prognosis
Physiologic or psychological comorbidities
Likelihood that the patient will be able to resume an active and relatively normal lifestyle following transplantation
Potential to comply with the posttransplant regimen
Level of psychosocial support
Patients with completed transplant evaluations are presented to a multidisciplinary selection committee for heart transplant listing consideration. If accepted, the team confirms insurance approval and then places the patient on the transplant waiting list.
Comprehensive education is provided to the patient and care partner at the time of listing.
While on the waiting list, patients undergo periodic reassessment.
The ISHLT-recommended schedule for heart transplant evaluation is shown in Table 9-10.10
Patients awaiting heart transplantation are assigned a status, which corresponds to how medically urgent it is that the candidate receive a transplant (Table 9-12).
TABLE 9-10 ISHLT-Recommended Schedule for Heart Transplant Evaluation and Waitlist Management
Repeat
Test
Baseline
3 Months
6 Months
9 Months
12 Months (and Yearly)
Complete H & P
X
Follow-up assessment
X
X
X
X
Weight/BMI
X
X
X
X
X
Immunocompatibility
ABO
X
Repeat ABO
X
HLA tissue typing
Only at transplant
PRA and flow cytometry:
X
>10%
Every 1-2 mo
VAD
Every 1-2 mo
Transfusion
2 wk after transfusion then per protocol
Assessment of heart failure severity
MVO2 with RER
X
X
Echocardiogram
X
X
RHC (vasodilator challenge as indicated)
X
X
X
ECG
X
X
Evaluation of multiorgan function
Routine lab work (BMP, CBC, LFT)
X
X
X
X
X
PT/INR more frequently per protocol if on VAD or Coumadin
X
X
X
X
X
Urinalysis
X
X
X
X
X
GFR (MDRD quadratic equation)
X
X
X
X
X
Urine sample for protein excretion
X
X
X
X
X
PFT with arterial blood gases
X
CXR (PA and lateral)
X
X
Abdominal ultrasound
X
Carotid Doppler (if indicated or > 50 y)
X
ABI (if indicated or > 50 y)
X
DEXA scan (if indicated or > 50 y)
X
Dental examination
X
X
Ophthalmologic examination (if diabetic)
X
X
Infectious serology and vaccination
Hep B surface Ag
X
Hep B surface Ab
X
Hep B core Ab
X
Hep C Ab
X
HIV
X
RPR
X
HSV IgG
X
CMV IgG
X
Toxoplasmosis IgG
X
EBV IgG
X
Varicella IgG
X
PPD
X
Flu shot (yearly)
X
Pneumovax (every 5 y)
X
Hep B immunizations 1, 2, and 3
X
Hep B surface Ab (immunity)
6 wk after third immunization
Preventive and malignancy
Stool for occult blood × 3
X
X
Colonoscopy (if indicated or > 50 y)
X
Mammography (if indicated or > 40 y)
X
X
Gyn/PAP (if indicated ≥18 y sexually active)
X
X
PSA and digital rectal exam (men >50 y)
X
X
General consultations
Social work
X
Psychiatry
X
Financial
X
Neurologic/psychiatric (if applicable)
X
ABI, ankle-brachial index; BMI, body mass index; BMP, basic metabolic panel; CBC, complete blood count; CMV, cytomegalovirus; CXR, chest x-ray; DEXA, dual-energy x-ray absorptiometry; EBV, Epstein-Barr virus; ECG, electrocardiogram; GFR, glomerular filtration rate; GYN, gynecology; H & P, history and physical; Hep B core Ab, hepatitis B core antibody; Hep B surface Ab, hepatitis B surface antibody; Hep B surface Ag, hepatitis B surface antigen; Hep C Ab, hepatitis C antibody; HIV, human immunodeficiency virus; HLA, human leukocyte antigen; HSV, herpes simplex virus; INR, international normalized ratio; LFT, liver function test; MDRD, modification of diet in renal disease; PA, posterior-anterior; PAP, Papanicolaou; PFT, pulmonary function test; PPD, purified protein derivative; PRA, panel reactive antibody; PSA, prostate-specific antigen; PT, prothrombin time; RER, respiratory exchange ratio; RPR, rapid plasma reagin; VAD, ventricular assist device.
Adapted from Mehra MR, Kobashigawa J, Starling R, et al. Listing criteria for heart transplantation: International Society for Heart and Lung Transplantation Guidelines for the care of cardiac transplant candidates—2006. J Heart Lung Transplantation. 2006;25(9):1024-1042.
TABLE 9-11 International Society for Heart and Lung Transplantation (ISHLT) Recommendations: Listing Criteria and Contraindications
Parameter
Recommendation
Maximal Cardiopulmonary Exercise Test MVO2 (on optimal medical therapy) with respiratory exchange ratio (RER) >1.05 and achievement of anaerobic threshold
Patients intolerant of β-blocker: Use cutoff for peak VO2 of ≤14 mL/kg/min to guide listing decision.
In presence of β-blocker: Use cutoff for peak VO2 of ≤12 mL/kg/min to guide listing decision.
Patients <50 y and women: Consider use of alternate standards in addition to peak VO2 to guide listing decision, including percent of predicted peak VO2 (≤50%).
If MVO2 is submaximal (RER < 1.05), consider use of ventilation equivalent of carbon dioxide (VE/VCO2) slope of > 35 to guide listing decision in obese patients (body mass index [BMI] > 30 kg/m2), consider adjusting VO2 to lean body mass.
Lean body mass-adjusted peak VO2 of < 19 mL/kg/min can serve as an optimal threshold to guide prognosis.
Heart Failure Survival Score (HFSS)
When CPX VO2 is ambiguous (e.g., peak VO2 > 12 and <14 mL/kg/min), consider HFSS as adjunct to guide listing decision for ambulatory patients.
(The HFSS is a multivariable predictive index that includes seven measurements: resting heart rate, mean blood pressure, ejection fraction, serum sodium level, peak VO2, intraventricular conduction delay, and presence of ischemic cardiomyopathy.)
Right heart catheterization
Right heart catheterization (RHC) should be performed on all candidates in preparation for listing for cardiac transplantation and annually until transplantation.
RHC should be performed at 3- to 6-month intervals in listed patients, especially in the presence of reversible pulmonary hypertension or worsening heart failure symptoms.
A vasodilator challenge should be administered when the pulmonary artery systolic pressure is ≥50 mm Hg and either the transpulmonary gradient (TPG) is ≥15 or the pulmonary vascular resistance is > 3 Wood units while maintaining a systolic arterial blood pressure > 85 mm Hg.
When an acute vasodilator challenge is unsuccessful, hospitalization with continuous hemodynamic monitoring should be performed, as often, the PVR will decline after 24-48 h of treatment consisting of diuretics, inotropes, and vasoactive agents.
If medical therapy fails to achieve acceptable hemodynamics and if the left ventricle cannot be effectively unloaded with mechanical adjuncts including an intra-aortic balloon pump (IABP) and/or left ventricular assist device (LVAD), it is reasonable to conclude that pulmonary hypertension is irreversible.
Patients intolerant of β-blocker: Use cutoff for peak VO2 of ≤14 mL/kg/min to guide listing decision.
In presence of β-blocker: Use cutoff for peak VO2 of ≤12 mL/kg/min to guide listing decision.
Patients <50 y and women: Consider use of alternate standards in addition to peak VO2 to guide listing decision, including percent of predicted peak VO2 (≤50%).
If CPX is submaximal (RER <1.05), consider use of ventilation equivalent of carbon dioxide (VE/VCO2) slope of >35 to guide listing decision in obese patients (body mass index [BMI] >30 kg/m2) and consider adjusting VO2 to lean body mass. Lean body mass-adjusted peak VO2 of <19 mL/kg/min can serve as an optimal threshold to guide prognosis.
Heart Failure Survival Score (HFSS)
When CPX VO2 is ambiguous (e.g., peak VO2 >12 and < 14 mL/kg/min), consider HFSS as adjunct to guide listing decision for ambulatory patients.
(The HFSS is a multivariable predictive index that includes seven measurements: resting heart rate, mean blood pressure, ejection fraction, serum sodium level, peak VO2, intraventricular conduction delay, and presence of ischemic cardiomyopathy.)
Right heart catheterization
Right heart catheterization (RHC) should be performed on all candidates in preparation for listing for cardiac transplantation and annually until transplantation.
RHC should be performed at 3- to 6-month intervals in listed patients, especially in the presence of reversible pulmonary hypertension or worsening heart failure symptoms.
A vasodilator challenge should be administered when the pulmonary artery systolic pressure is ≥50 mm Hg and either the transpulmonary gradient (TPG) is ≥15 or the pulmonary vascular resistance is >3 Wood units while maintaining a systolic arterial blood pressure >85 mm Hg.
When an acute vasodilator challenge is unsuccessful, hospitalization with continuous hemodynamic monitoring should be performed, as often, the PVR will decline after 24-48 h of treatment consisting of diuretics, inotropes, and vasoactive agents.
If medical therapy fails to achieve acceptable hemodynamics and if the left ventricle cannot be effectively unloaded with mechanical adjuncts including an intra-aortic balloon pump (IABP) and/or left ventricular assist device (LVAD), it is reasonable to conclude that pulmonary hypertension is irreversible.
Pulmonary artery hypertension and elevated PVR
Should be considered as a relative contraindication to cardiac transplantation when the PVR is >5 Wood units or the PVR index is > 6 or the TPG exceeds 16-20 mm Hg.
If the pulmonary artery systolic pressure exceeds 60 mm Hg in conjunction with any of the preceding three variables, the risk of right heart failure and early death is increased.
If the PVR can be reduced to ≤2.5 with a vasodilator but the systolic pressure falls < 85 mm Hg, the patient remains at high risk of right heart failure and mortality after heart transplantation.
Age
Patients should be considered for cardiac transplantation if they are ≤70 y of age.
Carefully selected patients >70 y of age may be considered for cardiac transplantation. For centers considering these patients, the use of an alternate-type program (e.g., use of older donors) may be pursued.
Cancer
Patients with preexisting neoplasms: Collaboration with oncologists is recommended to stratify each patient with regard to risk of tumor recurrence.
Cardiac transplantation should be considered when tumor recurrence is low based on tumor type, response to therapy, and negative metastatic workup. The specific amount of time to wait to transplant after neoplasm remission will depend on the aforementioned factors and no arbitrary time period for observation should be used.
Obesity
Pretransplant BMI >30 kg/m2 or percent ideal body weight (PIBW) >140% are associated with poor outcome after cardiac transplantation. For obese patients, weight loss is recommended to achieve a BMI of <30 kg/m2 or PIBW of <140% before listing for cardiac transplantation.
Diabetes
Diabetes with end-organ damage other than nonproliferative retinopathy or poor glycemic control (glycosylated hemoglobin [HbA1c] > 7.5) despite optimal effort is a relative contraindication for transplant.
Renal dysfunction
Renal function should be assessed using estimated glomerular filtration rate (eGFR) or creatinine clearance under optimal medical therapy. Evidence of abnormal renal function requires further investigation, including renal ultrasonography, estimation for proteinuria, and evaluation for renal artery disease, to exclude intrinsic renal disease. It is reasonable to consider the presence of irreversible renal dysfunction (eGFR < 40 mL/min) as a relative contraindication for heart transplantation alone.
Cerebrovascular disease
Clinically severe cerebrovascular disease, which is not amenable to revascularization, may be considered a contraindication to transplantation.
Peripheral vascular disease (PVD)
PVD may be considered as a relative contraindication to transplantation when its presence limits rehabilitation and revascularization is not a viable option.
Tobacco use
Education on the importance of tobacco cessation and reduction in environmental or secondhand exposure should be performed before the transplant and continue throughout the pre- and posttransplant periods.
It is reasonable to consider active tobacco smoking as a relative contraindication to transplantation. Active tobacco smoking during the previous 6 mo is a risk factor for poor outcomes after transplantation.
Substance abuse
A structured rehabilitation program may be considered for patients with recent (24 mo) history of alcohol abuse if transplantation is being considered.
Patients who remain active substance abusers (including alcohol) should not receive heart transplantation.
Psychosocial assessment
Psychosocial assessment should be performed before listing for transplantation. Evaluation should include an assessment of the patient’s ability to give informed consent and comply with instruction including drug therapy, as well as assessment of the support systems in place at home or in the community.
Mental retardation or dementia may be regarded as a relative contraindication to transplantation.
Poor compliance with drug regimens is a risk factor for graft rejection and mortality. Patients who have demonstrated an inability to comply with drug therapy on multiple occasions should not receive transplantation.
Adapted from Mehra MR, Kobashigawa J, Starling R, et al. Listing criteria for heart transplantation: International Society for Heart and Lung Transplantation guidelines for the care of cardiac transplant candidates—2006. J Heart Lung Transplantation. 2006;25(9):1024-1042.
There are four statuses for patients on the heart transplant waiting list:
Status 1A patients are typically admitted to the listing transplant center hospital (with the exception for 1A(b) candidates) and has at least one of the following devices or therapies in place:
Who are in the intensive care unit on life support (ventilator, intra-aortic balloon pump) and/or high-dose intravenous (IV) medications with a pulmonary artery catheter use to titrate therapy to optimize heart function.
Who have had a ventricular assist device (VAD) or ECMO to support their heart function or have a device-related complication.
An exception may be the outpatient with a VAD who is allotted 30 days of 1A time following the VAD implant.
Another exception is the electrically unstable patient deemed appropriate for the 1A status following a regional United Network for Organ Sharing (UNOS) board review.
Examples of Status 1B patients include patients who are
Receiving non-ICU or home continuous IV inotropic therapy
On a VAD (not using the 30 days of status 1A time)
Status 2 patients are patients who do not meet the criteria for status 1A or Status 1B. Most often, these patients are waiting at home for a donor heart and are taking oral heart failure medications.
TABLE 9-12 Heart Transplantation Status: Organ Procurement and Transplantation Network Definitions/Criteria
1A
A patient listed as status 1A is admitted to the listing transplant center hospital (with the exception for 1A(b) candidates) and has at least one of the following devices or therapies in place:
(a) Mechanical circulatory support for acute hemodynamic decompensation that includes at least one of the following:
(i) Left and/or right ventricular assist device implanted. Candidates listed under this criterion may be listed for 30 d at any point after being implanted as status 1A once the treating physician determines that they are clinically stable. Admittance to the listing transplant center hospital is not required.
(ii) Total artificial heart
(iii) Intra-aortic balloon pump
(iv) Extracorporeal membrane oxygenator (ECMO)
Qualification for status 1A under criterion 1A(a)(ii), (iii), or (iv) is valid for 14 d and must be recertified by an attending physician every 14 d from the date of the candidate’s initial listing as status 1A to extend the status 1A listing.
(b) Mechanical circulatory support with objective medical evidence of significant device-related complications such as thromboembolism, device infection, mechanical failure, and/or life-threatening ventricular arrhythmias. Other complications: Pump thrombus, persistent hemolysis, persistent bleeding, RV failure can petition using a regional board review. (Candidate sensitization is not an appropriate device-related complication for qualification as status 1A under this criterion). Admittance to the listing center transplant hospital is not required. Qualification for status 1A under this criterion is valid for 14 d and must be recertified by an attending physician every 14 d from the date of the candidate’s initial listing as status 1A to extend the status 1A listing.
(c) Continuous mechanical ventilation. Qualification for status 1A under this criterion is valid for 14 d and must be recertified by an attending physician every 14 d from the date of the candidate’s initial listing as status 1A to extend the status 1A listing. (d) Continuous infusion of a single high-dose intravenous inotrope (e.g., dobutamine ≥ 7.5 mcg/kg/min or milrinone ≥ 0.50 mcg/kg/min) or multiple intravenous inotropes, in addition to continuous hemodynamic monitoring of left ventricular filling pressures; qualification for status 1A under this criterion is valid for 7 d and may be renewed for an additional 7 d for each occurrence of a status 1A listing under this criterion for the same patient. VASODILATOR (nitroglycerine/Nipride) infusions do not qualify as inotropes.
1B
A patient listed as status 1B has at least one of the following devices or therapies in place:
(a) Left and/or right ventricular assist device implanted
(b) Continuous infusion of intravenous inotropes
A patient who does not meet the criteria for status 1A or 1B may be assigned to any desired status upon application by his/her transplant physician(s) and justification to the applicable Regional Review Board that the candidate is considered, using accepted medical criteria, to have an urgency and potential for benefit comparable to that of other candidates in this status as defined above. The justification must include a rationale for incorporating the exceptional case as part of the status criteria. A report of the decision of the Regional Review Board and the basis for it shall be forwarded for additional review by the Thoracic Organ Transplantation and Membership and Professional Standards Committees to determine consistency in application among and within all regions and continued appropriateness of the candidate status criteria.
2
A patient who does not meet the criteria for status 1A or 1B is listed as status 2.
7
A patient listed as status 7 is considered temporarily unsuitable to receive a thoracic organ transplant (on-HOLD).
Adapted from OPTN policy 3.7.3.
Status 7 patients are temporarily inactive on the heart transplant waiting list. An example of a status 7 patient would be one who
Is too sick to undergo transplantation (e.g., a patient who develops an infection and cannot undergo transplant surgery until the infection has cleared)
Is too well for transplantation
FIGURE 9-3 Adult heart transplantation survival by era January 1982 through June 2012. (Lund L, Edwards L, Kucheryavaya A, et al. The registry of the International Society for Heart and Lung Transplantation: thirty-first official adult heart transplant report—2014. International Society Heart Lung Transplant. 2014;33 (10):996-1008. Accessed September 10, 2015.)
Has lost health care insurance
Requests temporary inactive status
Patients status on the waiting list may change over time—depending on their medical condition and current needs.
Per the Scientific Registry of Transplant Recipients (SRTR) 2012 Annual Data Report, patient survival rates for adult US patients undergoing heart transplantation are as follows28:
1-year patient survival from 2005 to 2007: 88%
3-year patient survival from 2007 to 2010: 81%
5-year patient survival from 2005 to 2010: 75%
10-year patient survival from 2000 to 2010: 56.6%
Median overall patient survival from 1982 to 2012: 11 years or 14 years if the patient survives beyond the first-year posttransplant (n = 108,343; Figure 9-3).
Current 1- and 5-year ISHLT Registry patient survival rates are approximately 84.5% and 72%, respectively, for adult patients undergoing transplantation between 2006 and June 2011 (n = 18,896)28
 FIGURE 9-4 ISHLT diagnoses for patients who underwent heart transplantation between January 2006 and June 2012. (Lund L, Edwards L, Kucheryavaya A, et al. The registry of the International Society for Heart and Lung Transplantation: thirty-first official adult heart transplant report—2014. Int Soc Heart Lung Transplant. 2014;33(10):996-1008. Accessed September 10, 2015.) |
VII. EDUCATION FOR PATIENTS/CAREGIVERS AWAITING HEART TRANSPLANTATION
Description of and rationale for preoperative tests and procedures
Postoperative course (e.g., length of stay in intensive care unit [ICU] and intermediate care unit, progressive ambulation, use of incentive spirometer)
Lines that will be inserted (e.g., intravenous [IV] lines, pulmonary artery catheter, arterial line, urinary catheter, chest tubes, drains, pacing wires, endotracheal tube, naso- or orogastric tube)
Incisional care
Pain management plan
Activity limitations, lifestyle, and body image changes
Medications and side effects: with extra emphasis on the triple immune suppression medications
VIII. PREPARATION OF PATIENT FOR SURGERY26
Chest radiograph
Laboratory tests: Complete blood cell (CBC) count, complete metabolic profile (renal and hepatic function tests, electrolyte panel), coagulation tests, urinalysis, panel reactive antibodies (PRA), viral serologies
Recipient/donor prospective crossmatch (if required)29
A crossmatch may be indicated if the potential recipient’s PRA is >10% before transplant, indicating a higher risk for rejection if the recipient has unacceptable antibodies to the donor’s HLA antigens. See the Basics in Transplant Immunology chapter for additional information.
Accepting a graft from a donor that has antigens to which the recipient has antibodies could result in a positive crossmatch and may cause antibody-mediated rejection.
Several bioassays are used to detect circulating donor-specific antibodies (DSA) before or after transplant with the following sensitivities:
Multiplex bioassay using magnetic beads and lasers to identify unacceptable antigens or donor-specific antibodies: 93%
Complement-dependent cytotoxicity: 43%
Basic flow cytometry uses cell surface stains to detect antibodies: 43%
Enzyme-linked immunosorbent assay: 21%
Studies have shown that recipients who are highly sensitized prior to transplantation are more likely to develop DSA within the first 60 days posttransplantion; therefore, close monitoring is advised during this critical period.30
Obtain blood type and crossmatch per protocol
Blood products: (e.g., packed red blood cells, fresh frozen plasma, platelets) before, during, and after surgery are often required to correct coagulation abnormalities and replace intraoperative blood volume loss.
Leukocyte-depleted blood is ordered in some centers.
Leukocytes are removed by filtration of platelets and red blood cell concentrates that can lead to sensitization.
Giving leukopoor blood also reduces risk for cytomegalovirus (CMV) infection for patients with CMV-negative serologies.
CMV-negative blood is ordered for CMV-negative patients.
Giving CMV-positive blood (or an allograft from a CMV-seropositive donor) to a CMV-seronegative recipient increases the immunosuppressed recipient’s risk of contracting CMV disease.
Electrocardiogram: Particularly in patients who will have a repeat sternotomy; abnormal findings alert the anesthesiologist and surgeon to potential cardiac problems that may arise before cardiopulmonary bypass (CPB) is initiated.
Oral preoperative medications may be administered with a small sip of water.
ICD is deactivated at some point prior to surgery because the electrocautery used during the procedure can cause the device to discharge unexpectedly.
Fresh frozen plasma or phytonadione (vitamin K) if patient has been on anticoagulant therapy
Immunosuppressant(s)
Antianxiety agent(s)
Prophylactic antimicrobial therapy
TABLE 9-13 Examples of Desensitization Therapies | ||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||||||
Plasmapheresis
Mechanical removal of circulating antibodies may be used in highly sensitized patients to reduce the risk of allograft rejection preoperatively on the day of transplant (Table 9-13).29,30,31
Plasmapheresis can also be done to desensitize (remove unacceptable antibodies) the patient while on the waiting list or prior to transplant to reduce antibodies and increase likelihood of finding a negative crossmatch. It can be combined with the administration of intravenous immunoglobulin (IVIG).29
Rituximab (Rituxan): A monoclonal antibody to CD20 that is used to desensitize patients prior to heart transplantation. Rituximab depletes B lymphocytes through complement-dependent cytotoxicity and can be used instead of, or in addition to, plasmapheresis.31
Long-term data regarding the use of pretransplant allosensitization with rituximab or plasmapheresis in the highly sensitized transplant recipient have shown an increase in antibody-mediated rejection (AMR) and posttransplant coronary artery vasculopathy (CAV) and a decrease in overall graft survival. Studies are small and more data and experience are needed with this complicated population of patients.29
Bortezomib (Velcade) is a 23S proteosome inhibitor used in the treatment of multiple myeloma. It may be used in conjunction with plasmapheresis and rituximab for desensitization.32
Give patient/family opportunity to ask questions or verbalize their concerns.
Approximate time surgery will begin and duration of surgery (typically 4 to 8 hours)
Duration of surgery is typically longer if the recipient has had prior cardiac surgery, including implantation of a ventricular assist device.
Location of family waiting room
Provision of periodic updates by surgical team member
Location of the postanesthesia care unit (PACU) and/or ICU
Make certain that ICD is turned back on.
Make certain that patient is adequately anticoagulated if anticoagulation had been reversed.
Provide emotional support to patient and family.
Explain reason for cancelation of surgery.
Given the long waiting times for donor hearts, patient and family are typically very distraught over this “missed opportunity” and often wonder if another donor heart will be found in time.
Allow patient and family opportunity to express their emotions and disappointment.
If needed, arrange consultation with mental health and/or spiritual care provider.
IX. SURGICAL PROCEDURE
Large-bore peripheral lines
Hemodynamic monitoring lines (e.g., pulmonary artery catheter, arterial line) that will facilitate intra- and postoperative monitoring of
BP
Pulmonary artery pressure
PCWP (if ordered)
Central venous pressure (CVP)
Arterial blood gases (ABG)
CO/cardiac index (CI)
Foley catheter to monitor urine output
Naso- or orogastric tube to decompress the stomach and remove secretions
Chest tubes
Median sternotomy
Cuffs of the recipient’s native right and left atria are sutured to the donor right and left atria; donor aorta is sutured to recipient’s aorta; donor pulmonary artery is sutured to recipient’s pulmonary artery.
The donor heart is denervated.
With explanation of the donor heart, the sympathetic and parasympathetic nervous system fibers are severed (see “Denervation of the Cardiac Allograft”).
The recipient’s remaining native atrial tissue may still have electrical activity; however, these impulses do not cross the suture line.
Disadvantages of biatrial technique are related to the large and anatomically abnormal atria created during the surgery and include the risk of
Mitral and tricuspid valve regurgitation
Thrombus formation within the atria
Tachydysrhythmias
Persistent sinus node dysfunction requiring a permanent pacemaker
Biatrial technique is shown in Figure 9-5. Anastomoses include left atrium, right atrium, pulmonary artery, and aorta.
More commonly used.
Leaves recipient with more anatomically normal atria.
Intact donor RA is preserved; anastomoses are at recipient’s superior and inferior vena cava; left atrial cuff is reduced in size to a small area around the pulmonary veins.
Advantages:
Preserved sinoatrial (SA) node function
Decreased sinus node dysfunction
Decreased incidence of atrial dysrhythmias and mitral and tricuspid regurgitation.34
Disadvantages: Longer surgical procedure prolongs ischemic time.
Bicaval technique for orthotopic heart transplantation is shown in Figure 9-5.
Heterotopic transplantation is a procedure in which the donor heart is “piggybacked” onto the recipient’s native heart.
This procedure was first successfully performed in 1974.37 During the 1970s, it was the primary method of heart transplantation due to the ability of the recipient’s native heart to maintain cardiac function during acute rejection episodes.
With the advent of cyclosporine and improved outcomes with orthotopic heart transplantation, use of the heterotopic technique subsequently waned.38
More recently, heterotopic heart transplantation has increased in some centers owing to a number of factors, including
Increased number of large (>80 kg) candidates with refractory pulmonary hypertension
Underuse of small donor hearts and marginal allografts
Small donor pool in some areas of the world
Advantages of heterotopic transplantation include38
More lenient size matching between recipient and potential donor
Ability of recipient’s native heart to maintain hemodynamic stability during acute rejection episodes
Prevention of RV failure in recipients with severe pulmonary hypertension
Disadvantages of heterotopic transplantation include38
Continued pathology of native heart (e.g., ischemic disease, HF)
Difficulty in performing EMB
Persistent angina in recipients with ischemic cardiomyopathy
Need for anticoagulation in the setting of hypokinesis and clot formation
Pulmonary complications associated with compression and subsequent atelectasis of the right lung by the heterotopically placed donor heart
Example of a heterotopic heart transplant technique is shown in Figure 9-6.
 FIGURE 9-5 Native cardiectomy and donor graft preparation. A. Recipient pericardium after institution of cardiopulmonary bypass and ascending aortic occlusion with caval snares secured. The diseased native heart can then be safely excised by transecting the recipient aorta and pulmonary artery, and the atria can be divided as appropriate for intended implant technique. Shown is the right atrial incision for the traditional Lower/Shumway right atrial cuff. B. Posterior view of the explanted donor heart, indicating various incisions used for atrial cuff preparation. Donor atrial cuff incisions made in preparation for traditional Lower/Shumway biatrial implant are indicated by the heavy gray dashed line. The superior vena cava (SVC) is ligated or oversewn. Right and left pulmonary vein (light gray dashed line) and superior vena cava (black dashed line) incisions are indicated for the total atrioventricular implant technique. For the bicaval technique, the donor SVC and inferior vena cava (IVC) are retained as for the total atrioventricular technique (black dashed line), and the donor left atrial cuff trimmed as for the traditional biatrial approach (heavy gray dashed line). (Mulholland MW, Lillemoe KD, Doherty GM, et al. Greenfield’s Surgery: Scientific Principles and Practice. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.) |
X. DENERVATION OF CARDIAC ALLOGRAFT38
Bradyarrhythmias may be observed in the immediate postoperative period; chronotropic support with isoproterenol (Isuprel) or pacing may be temporarily required.
Unique response to activity, exercise, and stressors such as hypovolemia, hypoxia, hemorrhage, and ischemia.
FIGURE 9-6 Heterotopic method of heart transplantation. The donor heart is anastomosed with a Dacron graft to the recipient’s heart, resulting in this ECG tracing. Note the “extra” QRS at an independent rate. (From Smeltzer SC, Bare BG. Brunner and Suddarth’s Textbook of Medical-Surgical Nursing. 10th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004:775.)
Heart transplant recipients have a higher than normal resting HR averaging 90 to 110 beats per minute (bpm).
See Table 9-14 for a comparison of normal (innervated) and denervated heart.
Response to vigorous physical activity and exercise
Recipients require a longer warm-up period before exercise so that circulating catecholamines and increased venous return can increase HR.
Because the denervated heart’s response to activity is slow, it is essential to have the patient do appropriate warm-up exercises (e.g., 5 to 10 minutes of leg pumping, ankle rotations) prior to engaging in activity (getting out of bed, ambulating). Failure to do so can result in orthostatic hypotension.
TABLE 9-14 Comparison of Normal and Denervated Heart
Factor
Normal Heart
Denervated Heart
Parasympathetic innervation
Resting HR 60-100 bpm due to inhibitory effect of parasympathetic stimulation
No parasympathetic stimulation Resting HR = 90-110 bpm30
Sympathetic innervation
Direct sympathetic stimulation that automatically increases CO with exercise
No direct sympathetic stimulation; other mechanisms increase CO with exercise:40
Early in exercise: ↑ venous return augments preload and ↑ CO
Later in exercise: inotropic and chronotropic effects of catecholamines released from noncardiac sites results in ↑ CO
bpm, beats per minute; CO, cardiac output; HR, heart rate.
Similarly, recipients require a longer cooldown after exercise so that HR can gradually decrease as circulating catecholamines dissipate.
Patients should not abruptly stop vigorous physical activity. Instead, they should gradually decrease their level of activity.
The denervated heart does not respond well to stress that requires an abrupt increase in HR (e.g., hypoxia, hemorrhage, hypovolemia) in order to maintain or increase CO.
The denervated heart will have an altered response to certain cardiac drugs. In particular, atropine is not useful in the setting of bradycardia, because atropine’s mechanism of action is to block input from the parasympathetic nerves (see “Response of Denervated Cardiac Allograft to Medications”).
Isoproterenol (Isuprel) may be used to treat bradycardia because it directly stimulates cardiac adrenergic receptors (see “Hemodynamic Monitoring and Support”).
Theophylline (Theo-Dur) and terbutaline may also be considered.
Terbutaline, dosed orally, may also be used for a period of time postoperatively to ensure adequate heart rate.
The normal diurnal variation in blood pressure is eliminated.
The transplanted heart lacks afferent innervation.39 Although there is some evidence that partial reinnervation may develop over time,39,40 most recipients with myocardial ischemia or infarction typically do not have angina, as there is no direct afferent sensory input.
Clinical manifestations of ischemia in heart transplant recipients include the sequelae of ischemia or infarction such as shortness of breath, increased fatigue, decreased ability to perform usual activities, etc.
However, it is important to teach recipients not to disregard angina, as angina can be a symptom of ischemia in some patients.
XI. ROUTINE POSTOPERATIVE MONITORING AND MAINTENANCE: EVALUATE OBJECTIVE CRITERIA41,42,43,44,45,46,47,48,49
Patient arrives in ICU sedated and intubated with
Dressings in place over sternal incision, pacemaker/ICD removal site, MCS exit cannula removal site
The surgical dressing is typically left in place for approximately 24 to 48 hours, unless bleeding from the surgical wound necessitates removal of the dressing.
Mediastinal, pericardial, and, usually, pleural drains
Mediastinal and pleural drains are typically placed to 20 cm of underwater seal suction48
Atrial and ventricular temporary epicardial pacing wires (see “Telemetry and Epicardial Pacemaker”)
Goals of nursing care:
Maintenance of graft function and hemodynamic stability
Ensuring proper ventilation and oxygenation
Maintenance (or recovery) of all organ system functions
Prevention or early recognition of complications
Patients are placed in protective isolation status per center protocol (see “Prevention of Infection”).
Systolic BP is typically maintained at 90 to 110 mm Hg.
HR is typically maintained at 100 to 120 bpm.
Hemodynamic monitoring includes
BP via an arterial line
Swan-Ganz catheter to monitor:
Pulmonary artery pressures
CVP
CO and CI
Mixed venous oxygen saturation (SvO2; normal: 60% to 80%)
Pulse oximetry
Obtain specific guidelines from the physician regarding acceptable hemodynamic parameters; monitor hemodynamic profile and notify physician if patient deviates from acceptable parameters.
Acceptable hemodynamic parameters differ from patient to patient and depend on a number of factors including
Preoperative conditions (e.g., pulmonary hypertension, renal insufficiency)
The intraoperative course
Preservation techniques
Ischemic time of the donor heart
Due to the incidence of RV dysfunction in the transplanted heart, maintaining an RA pressure of 5 to 12 mm Hg is recommended.42
It is important to monitor, document, and report trends.
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