Imaging Flashcards
An 82-year-old man with a history of hypertension, hyperlipidaemia and COPD presented from a nursing home for an emergent laparotomy for a ruptured appendix.
A transoesophageal echocardiography (TEE) probe was placed intraoperatively for
diagnosis and monitoring after several attempts at managing hypotension proved futile.
1. What are some of the benefits of using TEE in managing patients for non-cardiac surgery?
○ TEE can provide immediate and accurate haemodynamic measurement of cardiac function including cardiac output and left ventricular filling pressure, chamber preload, atrial interaction and pulmonary arterial pressures.
○ Doppler ultrasound principles are used to derive intracardiac flow across orifices and valves in order to calculate orifice area, stroke volume and cardiac output.
○ Intraoperative cardiac output measurement provides a tool for assessing global cardiac function. The information obtained from the cardiac output measurement can be used in guiding therapeutic decision during cardiac and non-cardiac surgery.
○ The use of TEE for cardiac output measurement thus provides a simple and reliable minimally invasive method of assessing cardiac function.
○ Intraoperatively, TEE can be used to diagnose or redefine the cause of haemodynamic instability and detect new or unsuspected pathology like valvular (stenosis or regurgitation) and other lesions.
- What physics principles underlie the calculation of valve area, stroke volume and cardiac output using TEE? (See Figs. 52.1, 52.2, 52.3, 52.4 and formula illustration)
○ Blood flow across valves and orifices of the heart can be obtained using the Doppler capabilities of echocardiography and applying the basic principle of physics and fluid dynamics.
○ According to the principles of physics and fluid dynamics,
Volume in a cylinder= cross-sectional area of the cylinder or vessel
× length of cylinder or vessel = pie r squared × L pr
○ Also, flow rate (Q) is calculated as
Flow rate Q= volume/t=Area×L/t = pie r squared ×L/t
where t is time for fluid to traverse from point A to B.
○ Using the law of conservation of mass (continuity equation) and assuming laminar flow,
Qª=Qb
○ The velocity (and distance L) that blood travels in a blood vessel can be measured by TEE using continuous or pulse wave Doppler. Continuous wave uses two crystals; one crystal continuously transmits ultrasound wave and the other crystal continuously receives ultrasound waves thus allowing for measurement of high-frequency Doppler velocities along the entire length of the ultrasound beam [1]. In contrast to continuous wave measurement, pulse wave measurements use one ultrasound crystal for both transmitting and receiving ultrasound waves. This allows for measurement of low-frequency Doppler velocity (v) from a specific region of blood flow.
○ Using either continuous or pulse wave Doppler allows for the measurement of velocity (v) and distance (measured by the echo machine as velocity time integral (VTI)). The VTI and v are obtained by tracing the area under the Doppler signal obtained. The VTI is also called the stroke distance that is the distance travelled by the sampled volume per heartbeat. Therefore, the pulse wave VTI is the distance travelled by a blood sample at a specific point in the LVOT, while the continuous wave VTI (usually measured across the aortic valve) is the longest distance travelled by blood across the aortic valve [1–3].
Intraoperative echo showed a severely calcified aortic valve with a left ventricular outflow tract diameter (LVOT) of 2.59 cm, an LVOT VTI of 17.5, maximum
LVOT velocity (Vmax) of 69.2 cm/s, aortic valve VTI of 152 cm and an aortic valve Vmax of 533 cm/s. The heart rate on the monitor was 97 beats/min. How would you calculate the stroke volume and cardiac out?
A 60-year-old-patient with a history of right upper lobe lung cancer, peripheral
vascular disease, and chronic bronchitis is scheduled for a transthoracic echocar-
diography as part of workup for lung resection. Echocardiography evaluation
revealed a severely calcified aortic valve, severe left ventricular hypertrophy, and a
low normal ejection fraction (EF 50%):
1. What is the etiology and pathophysiology of aortic stenosis?
Causes of aortic stenosis (AS) in adults:
(a) Degeneration of tricuspid valve—commonest, seen after 60 years age,
caused by generalized atherosclerosis
(b) Degeneration of bicuspid valve—seen before 60, fusion of right and left
cusps resulting in large anterior and small posterior cusp, associated with
aortic dissection, aneurysm and coarctation
(c) Rheumatic—commonest cause worldwide, usually associated with mitral
disease as well
(d) Outflow obstruction:
• Subvalvular—either membrane or hypertrophic obstructive cardiomyop-
athy (HOCM)
• Supravalvular—Williams syndrome
Aortic sclerosis, defined as valve thickening without obstruction to LV out-
flow, is present in 25% of adults over 65 years of age. Predisposing factors com-
mon to both aortic stenosis and sclerosis are hypertension, smoking, serum
low-density lipoprotein, and diabetes mellitus. Aortic sclerosis usually pro-
gresses to aortic stenosis in the presence of progressive inflammatory atheroscle-
rosis. Ten percent of patients with aortic sclerosis progress to AS within 5 years.
In the 2014 ACC/AHA guidelines on valvular disease, aortic sclerosis is consid-
ered part of the AS continuum with sclerosis assigned stage A (at risk group).
How do you assess and grade aortic stenosis?
Diagnosis and assessment of severity of AS made on the basis of history, physi-
cal exam, and echocardiographic findings. Patients with severe aortic stenosis
(AS) usually present with angina, syncope, sudden death, or heart failure.
Physical exam may reveal a crescendo-decrescendo ejection murmur. ECG will
show signs of left ventricular hypertrophy and left atrial enlargement.
Two-dimensional echocardiography with Doppler evaluation (TTE or TEE) is
the test of choice to confirm the diagnosis of AS and assess severity and also note
the presence of coexisting diseases such as aortic regurgitation, mitral stenosis,
mitral regurgitation, aortic root dilation, and coronary artery disease (Fig. 53.1).
The peak velocity and mean pressure gradient across the aortic valve are mea-
sured by means of Doppler interrogation of the aortic valve (Fig. 53.2). Accurate
Doppler measurement of aortic valve velocity (and pressure) requires a near par-
allel alignment of the ultrasound beam to the aortic valve. The normal aortic
valve area is approximately 3.0–4.0 cm2. The velocity and pressure gradients
across the aortic valve are flow dependent. In patients with low ejection fraction,
dobutamine or exercise stress echo may be needed to confirm the diagnosis. In
the 2014 guidelines, severity of AS was divided into 4 stages (A, B, C, and D)
based on valve anatomy, valve hemodynamics, hemodynamic consequence, and
symptoms [1] (Table 53.1).
What is the natural history of patients with aortic stenosis?
○ Patients with aortic stenosis usually present when symptoms become severe enough to disrupt normal daily activity. Prior to that, morbidity and mortality are very low.
○ The rate of progression to severe aortic stenosis varies, but in general it has been shown that in patients with at least moderate aortic stenosis, jet velocity across the
aortic valve increases by 0.3 m/s per year, mean gradient increases by 7 mmHg per year, and AVA decreases by 0.1 cm2 per year.
○ Patients with symptomatic or
severe aortic stenosis present with angina, dyspnea, lightheadedness, syncope, and heart failure. Sudden death is a feared complication of severe aortic stenosis, and, although rare, it has been reported to occur without symptoms.
○ Average survival in patients with symptomatic aortic stenosis is 30–50% at 2 years. Patients with
asymptomatic severe AS require close monitoring in order to detect sudden changes in symptoms. Patients with mild-to-moderate aortic stenosis will not have symptoms of the disease, but due to the unpredictable disease progression, it is mandatory for these asymptomatic patients to have regular clinical follow-up and evaluation for
development of symptoms and disease progression. During these follow-ups,patients should be educated on the signs and symptoms of disease progression such
as exercise intolerance, exertional chest discomfort, dyspnea, and syncope.
. What interventions are available for patients with aortic stenosis
Appearance of symptoms is the most important indication for intervention in patients with aortic stenosis.
○ There are no specific medical therapies to treat or slow the progression of aortic stenosis.
° It is recommended to treat hypertension in patients with increased risk of developing AS (stages B and C). Hypertension is prevalent in patients with AS and has been shown to be a risk factor for AS and also increase the morbidity and mortality risk associated with AS.
°The treatment is started at low dose, and patients should be monitored closely by experienced cardiologist to avoid complications associated with the disease state or treatment in these high-risk patients.
° Angiotensin-converting enzyme (ACE) inhibitors, diuretics, and
vasodilators can be used in the acute setting in patients with severe decompensated AS. The use of these medications may require invasive hemodynamic monitoring.
○ Aortic valve replacement (AVR) is the only definite treatment for patient with AS. Early surgical intervention has been shown to decrease mortality in patients with
severe AS. Decision to operate should be based on symptoms, valve anatomy, and hemodynamics.
°The ACC/AHA guideline recommends surgical AVR for all
patients who meet an indication for AVR with low or intermediate surgical risk. Major indications for surgical AVR (class I recommendation) are severe symptomatic AS, asymptomatic severe AS with LVEF <50%, asymptomatic severe AS in patients undergoing CABG, other heart surgeries or surgery on the aorta.
° In patients with moderate AS undergoing other cardiac surgery, it is reasonable to perform surgical AVR if the aortic velocity is between 3 and 3.9 m/s or the mean pressure gradient is between 20–39 mmHg (class IIa recommendation). These patients are likely to have symptoms of the disease within 5 years due to the progressive nature of aortic stenosis [2].
○ Transcatheter aortic valve replacement (TAVR) is a minimally invasive surgical procedure for replacing the aortic valve. At present, it is indicated in patients with severe AS who are high risk for open surgical replacement of the aortic
valve.
° It involves placing a valve mounted on balloon at the tip of a catheter over a diseased native aortic valve. The catheter is fed through either the femoral artery or through the apex of the heart which require a small incision to be made
on the left chest wall.
° According to the ACC/AHA 2014 guidelines on valvular disease, TAVR is recommended in AS patients with indications for AVR who have a high risk for open AVR, or a prohibitive surgical risk and a predicted post
TAVR risk greater than 12 months.
A 45-year-old Caucasian female with a recent history of breast cancer status post-
chemotherapy and radiation therapy was admitted with high-grade fever, slurred
speech, back pain, and petechial rash. Surveillance cultures had been inconclusive
with one of three samples being positive for coagulase-negative Staphylococcus
aureus. Transthoracic echocardiography, performed as part of initial workup,
showed no valvular vegetation, preserved ejection fraction (55%), and mild aortic regurgitation. A diagnosis of infective endocarditis was suspected, and despite treat-
ment with antibiotics, the patient continued to have intermittent high-grade fever
and signs and symptoms of congestive heart failure. Transesophageal echocardiog-
raphy performed 7 days’ post-presentation showed a large mobile mass on the aortic
valve, severe aortic regurgitation with a depressed ejection fraction of 40% (see
Figs. 54.1, 54.2, and 54.3). Therefore, cardiothoracic surgery was consulted for
evaluation for possible valve replacement surgery
1. What are the risk factors for infective endocarditis?
The following patients present a high risk for infective endocarditis [1–9]:
(a) Male, elderly (age > 60)
(b) Prior history of prior IE
(c) Poor dental hygiene
(d) Patient undergoing dental procedures involving gingival tissues
(e) Patients with valvular heart disease (e.g., rheumatic valvular disease)
(f) Patients with uncorrected or partially corrected congenital heart disease
(g) IV drug use
(h) Prosthetic valves
(i) Immunosuppressed patient
(j) Patients with history of diabetes
(k) Patients with intracardiac devices
(l) Patients undergoing hemodialysis
Explain the pathophysiology of infective endocarditis?
Pathophysiology:
(a) IE occurs when bacteria or fungi invade sterile platelet-rich thrombus at sites
of injury in the endocardium.
(b) Sources of bacteria include the skin, oral cavity, mucosal surfaces, or sites of
focal infection.
(c) Infection results in invasion of the thrombus and destruction of the underly-
ing valvular and endocardial tissues.
(d) Bacteria usually resistant to the complement system of the body.
(e) Common bacterial species: Staphylococcus, Streptococcus, Enterococci,
and HACEK group (Haemophilus, Actinobacillous, Corynebacterium,
Eikenella, and Kingella).
Describe the clinical manifestations of infective endocarditis?
Infective endocarditis can affect all organ systems of the body [1–9]:
(a) Nonspecific symptoms: fever (most common symptoms), chills, sweats, headaches, weight loss, back pain, myalgia arthralgia, cough, and pleuritic chest pain
(b) Other symptoms highly specific for IE: cardiac murmur (85% of patients), splinter hemorrhage in nail beds, petechiae on skin and mucous membranes, Janeway lesions (nontender macules on palm and sole), Roth spots (hemorrhagic lesions on retina), and Osler nodes (tender nodules on fingers and toes)
(c) Cardiac complications: valvular insufficiency, congestive heart failure (30–40% of IE patients), and periannular and intraventricular abscesses (can result in intracardiac fistulas), cardiac arrhythmias (usually the result of peri-annular abscesses)
(d) Vascular-embolic complications: septic emboli (15–35% of IE patients), mycotic aneurysm, and vertebral osteomyelitis
(e) Neurologic complications (mostly from vascular embolic events): brain
abscess, embolic stroke, and cerebral hemorrhage
(f) Renal complications: kidney infarct from septic emboli and glomerulonephritis (caused by immune complexes)
(g) Pulmonary complications (commonly seen in right heart IE): septic pulmonary emboli and pyopneumothorax
How do you diagnose infective endocarditis?
The modified Duke Criteria is the most common guideline used in the diagnosis
of infective endocarditis. Pathological and clinical information obtained during
workup have been divided into major and minor criteria (adapted with permis-
sion from the ACC/AHA 2014 Guidelines for Management of Valvular Heart
Disease) [8]:
(a) Major criteria:
• Blood culture positive for IE: at least two positive cultures of blood sam-
ples drawn >12 h apart or all three or a majority of ≥4 separate cultures
of blood (with first and last sample drawn at least 1 h apart)
• Single positive blood culture for Coxiella Burnetii or anti-phase 1 IgG
antibody titer ≥1:800
• Evidence of endocardial involvement
• Echocardiogram positive for IE
(b) Minor criteria
• Predisposing heart condition
• IV drug use
• Fever (temperature > 38 °C)
• Vascular phenomena including major arterial emboli, septic pulmonary
infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hem-
orrhages, and Janeway lesions
• Immunological phenomena including glomerulonephritis, Osler nodes,
Roth spots, and rheumatoid factor
• Positive blood culture but does not meet a major criterion as noted above
(c) The criteria further stratify the diagnosis of IE into definite, possible, or
rejected based on whether a patient exhibits a set of major and/or minor
clinically defined characteristics (adapted with permission from the ACC/
AHA 2014 Guidelines for Management of Valvular Heart Disease):
• Definite IE:
Pathological criteria: culture demonstrated microorganism or histology
showing intracardiac abscess
Clinical criteria: two major criteria or one major and three minor criteria
or five minor criteria
• Possible IE:
One major criterion and one minor criterion or three minor criteria.
• Rejected IE:
Firm alternative diagnosis.
No pathological evidence of IE was found at surgery or autopsy after
antibiotic therapy for 4 days or less.
Resolution of clinical manifestations occurs after ≤4 days of antibiotic
therapy.
Clinical criteria for possible or definite infective endocarditis are not
met.
What is the role of TTE and TEE in the diagnosis of infective endocarditis?
Echocardiography is a major criterion in the diagnoses of infective endocarditis,
and therefore it should be performed in all patients with suspected IE [8]:
(a) Echocardiographic evidence of IE includes (see Figs. 54.1, 54.2, and 54.3):
• Valvular vegetation
• Associated valvular regurgitation
• Intracardiac mass
• Periannular abscess
(b) Transthoracic echocardiogram (TTE):
• Initial test of choice to identify vegetation and quantify hemodynamic
effect of IE.
• Good sensitivity and specificity (75% and ~100%, respectively).
• Absence of lesions on TTE does not rule out IE when there is high suspi-
cion of IE.
• Suboptimal TTE images may be seen in patients with chronic obstructive
pulmonary disease, previous thoracic and cardiovascular surgery, and
morbid obesity.
(c) Transesophageal echocardiogram (TEE):
• Generally, more sensitive for the diagnosis of TEE especially for pros-
thetic valves, paravalvular abscess, fistulas, and intracardiac devices.
• Specificity is slightly lower than TTE.
• Recommended as the initial test of choice when feasible.
• Recommended in cases of negative TTE but high suspicion of IE.
• Recommended for follow-up of patients with IE, small left-sided heart IE
and patients who develop progressive disease despite institution of anti-
microbial therapy.
What are the treatment options for patients with infective endocarditis?
Treatment: The mainstay of treatment for infective endocarditis is antibiotic,
often over weeks, with regular surveillance to gauge effectiveness of treatment.
(a) Factors that present a challenge during antibiotic treatment:
• Focal infection with high bacterial density
• Impaired immunity in the patient
• Slow rate of bacterial growth within a biofilm
• Low microorganism metabolic activity
(b) Choice of antibiotics must be based on the knowledge of the susceptibility
profile of the microorganism in the vegetation.
(c) Systemic antibiotics must be in concentrations high enough to counteract the
high density of bacterial in the vegetation.
(d) An expected infectious disease must be directly treated with antimicrobials
in IE patient.
(e) Valve replacement is recommended in the following cases:
• Large mobile vegetation greater than 10 mm in diameter
• Vegetation with associated regurgitation
• Paravalvular infection and/or annular abscess
• Penetrating intracardiac lesion
• Endocarditis with associated heart block and/or malignant arrhythmia
• Fungal vegetation
• Persistent bacteremia despite antibiotic treatment
Which are the guidelines on managing high-risk patients presenting for surgery?
- Antibiotic prophylaxis is recommended in the following highest-risk patients
only:
(a) Prosthetic heart valve
(b) Prior history of IE
(c) Dental procedures involving break in oral mucosa and gingival tissue
(d) Procedures in infected gastrointestinal and genitourinary tract
(e) Procedures on infected skin and integument
(f) Biopsy of the respiratory tract
(g) Unrepaired cyanotic congenital heart disease
(h) Repaired congenital heart disease with residual defects
Antibiotics for Recommendation for Dental Procedures [1]
(a) Patients who can take oral meds:
• Oral amoxicillin (adults 2 g, children 50 mg/kg)
(b) Patients unable to take oral meds:
• Ampicillin IV or IM (adults 2 g, children 50 mg/kg)
• Cefazolin IV (adults 1 g, children 50 mg/kg)
• Ceftriaxone IV (adults 1 g IV or IM, children 50 mg/kg)
(c) Patients allergic to penicillin (anaphylaxis, angioedema, urticaria):
• Oral azithromycin or clarithromycin (adult 500 mg, children 15 mg/kg)
• Oral clindamycin (adults 600 mg, children 20 mg/kg)
(d) Patients allergic to penicillin and unable to take oral medications:
• Clindamycin IV or IM (adults 600 mg, children 20 mg/kg)
• Vancomycin IV (adults 15 to 20 mg/kg, children 15 mg/kg)
