Book 4, Case 8=Cardiac ablation Flashcards
Rheumatic fever issues;
Can cause mitral stenosis with subsequent a fib
Concerns in a pt with A fib:
acute ischemic stroke, either embolic (atrial fibrillation or thrombotic material) or thrombotic (the patient’s diabetes mellitus, hypertension, and history of stroke suggest the possibility of cerebral vascular disease); ( 4) hemodynamic instability, secondary to chronic hypertension, atrial fibrillation, and possible mitral valve stenosis; (5) congestive heart failure, secondary to myocardial ischemia or the right ventricular pressure overload associated with mitral valve stenosis (again, the possibility of mitral valve stenosis is suggested by the patient’s history);
Causes of Atrial fibrillation
While the etiology of atrial fibrillation could be completely idiopathic, it is more often associated with a cardiac condition such as valvular disease, left ventricular hypertrophy, coronary artery disease, hypertension, cardiomyopathy, sick sinus syndrome, or pericarditis. Considering this patient’s hypercholesterolemia, diabetes mellitus, hypertension, obesity, increased age, tobacco use, and history of rheumatic fever, it is very likely that her atrial fibrillation is the result of coronary artery disease, hypertension, and/or mitral valve stenosis. Less frequently, there are non-cardiac factors that contribute to the development of atrial fibrillation, such as hyperthyroidism, pulmonary embolism, excessive alcohol consumption, or caffeine intake.
HCTZ MOA and what electrolyte does it lower?
Inhibits NaCl transport in distal convoluted tubule Can cause hypokalemia and hyponatremia
How does diltiazem work? Goals of tx in a fib? Should pt continue it day of surgery?
Diltiazem is used to control the heart rate in chronic A-fib by decreasing the rate of the SA node and by slowing conduction through the AV node. Diltiazem, like other calcium blockers, should be used with caution in patients with reduced ventricular function (heart failure) due to its negative inotropic affects. However, diltiazem produces significantly less myocardial depression than verapamil, and is the preferred drug in patients with systolic heart failure. Medical treatment for atrial fibrillation depends on the type, severity of symptoms, the underlying cause, and comorbid conditions. In general, the goal of treatment is threefold: (1) slow down the heart rate, (2) restore and maintain normal heart rhythm, and (3) prevent stroke by anticoagulation. The decision to continue her diltiazem preoperatively would depend on her underlying ventricular rate when not on a calcium channel blocker, her risk for myocardial ischemia, and the degree to which diltiazem may interfere with electrophysiologic mapping. Typically, anti-arrhythmic medications are discontinued to facilitate the induction of arrhythmias when mapping the conduction pathways and source of excitability. However, since calcium channel blockers control the ventricular rate by slowing conduction through the AV node, they have minimal effects on electrophysiologic mapping and should be continued perioperatively. Moreover, should she have mitral valve stenosis, an increase in ventricular rate, as may occur with the discontinuation of diltiazem, could lead to significantly decreased cardiac output and end-organ ischemia.
Indications for catheter ablation:
Indications for catheter ablation include: (1) symptomatic supraventricular tachycardia (SVT) due to atrioventricular nodal reentrant tachycardia (A VNRT), Wolff-Parkinson-White syndrome, unifocal atrial tachycardia, or atrial flutter; (2) atrial fibrillation with lifestyle-impairing symptoms and either inefficacy or intolerance of at least one antiarrhythmic agent; (3) symptomatic ventricular tachycardia; (4) patient preference; and (5) noncompliance with drug regimens.
What do you think is the cause of her syncopal episode? Does she need further evaluation?
What do you think is the cause of her syncopal episode? Does she need further evaluation? Given this patient’s chronic atrial fibrillation, history of stroke, and possible mitral valve stenosis (i.e. history of rheumatic fever and atrial fibrillation of unknown etiology), her recent syncopal episode is most likely secondary to cardiac arrhythmia and/or transient ischemic attack (TIA). However, since she is diabetic and has several risk factors for coronary artery disease, I would also consider the possibility of hypoglycemia or myocardial ischemia. Finally, I would give consideration to other potential causes of syncope, such as seizure, aortic stenosis, hypertrophic cardiomyopathy, vasovagal response, or vertigo. Additional work-up would be based on the suspected etiology of her syncope, and may include an electrocardiogram, an exercise stress test, an echocardiogram, carotid sinus message, or a tilt table test.
Pt with hx of of rheumatic fever with mitral stenosis, and moderate tricuspid regurgitation
This patient’s moderate tricuspid regurgitation is most likely secondary to rheumatic disease and/or the pulmonary hypertension that has most likely developed as a result of her mitral valve stenosis (other potential causes include infective endocarditis, carcinoid syndrome, tricuspid valve prolapse, and Ebstein’s anomaly). The restriction of flow through the stenotic mitral valve leads to increased left atrial pressures, which are then transmitted to the pulmonary circulation. Over time, chronically elevated pressures in the pulmonary circulation result in pulmonary vascular changes that lead to the development of irreversible pulmonary hypertension right ventricular pressure overload, compensatory right ventricular hypertrophy, and, eventually, right ventricular dilation. Finally, significant dilation of the right ventricle can lead to tricuspid regurgitation (also pulmonary valve regurgitation).
Tell me about grading of MS:
How does this patient’s tricuspid regurgitation affect your anesthetic
management?
Considering this patient’s moderate tricuspid regurgitation, I would
seek to avoid conditions that lead to decreased preload and/or increased right
ventricular after load, such as hypovolemia (decreased pre load), decreased systemic
vascular resistance (decreased preload), hypoxia (increased pulmonary artery
pressure), hypercarbia (increased pulmonary artery pressure), acidosis (increased
pulmonary pressure), and tachycardia (impaired left ventricular filling and increased
left atrial pressures lead to increased right ventricular afterload). Additionally, I
would: (1) avoid nitrous oxide, which could exacerbate pulmonary hypertension; (2)
ensure that any air in the intravenous lines is removed, recognizing that elevated right
atrial pressures and decreased left sided filling pressures place this patient at
increased risk for right-to-left shunting through a patent foramen ovale; (3) monitor
central venous pressures to guide fluid administration, monitor right ventricular
function, and detect changes in regurgitant volume; and ( 4) avoid excessive airway
pressures during mechanical ventilation (i.e. PEEP, high mean airway pressures),
which could lead to increased afterload and decreased preload.
Would you place a pulmonary artery catheter for this case?
What can you expect to be different about PAC in pt with TR?
Given her mitral valve stenosis and tricuspid regurgitation, utilizing a
pulmonary artery catheter to monitor pulmonary artery pressure (right ventricular
afterload), cardiac output, and systemic vascular resistance may prove valuable in
guiding fluid therapy, ensuring adequate preload, and maintaining cardiac output.
However, given the inaccuracies in pulmonary artery data associated with tricuspid
regurgitation and mitral valve stenosis, the difficulty of passing the catheter through
the regurgitant tricuspid valve (due to interference from the regurgitant wave), and
the increased risk of massive hemorrhage in the setting of pulmonary hypertension
(increased risk of pulmonary artery rupture) and an elevated INR (normal= 0.9-1.2), I
would not employ this method of monitoring for this patient.
If a pulmonary artery catheter were used, it would be important to recognize that, in
the setting of mitral valve stenosis and tricuspid regurgitation, (1) the pulmonary
capillary wedge pressure would overestimate the left ventricular diastolic pressure
(L VDP) by at least the amount of the mitral valve pressure gradient; (2) tachycardia
and elevated cardiac output increase the mitral valve pressure gradient, leading to an
increasing difference between the estimated and actual L VDP; and (3) thermodilution
cardiac output measurements are inaccurate (falsely elevated), due to a portion of the
cold injectate moving retrograde into the atrium rather than into the pulmonary artery.
Would you provide general anesthesia or MAC for this case? What are the
advantages of general anesthesia?
I wold do it under general. Here is what UBP says-use thi to your advantage when choosing general
Given the importance of maintaining adequate preload in this patient
with mitral valve stenosis and tricuspid regurgitation, I would prefer to perform this
case under MAC to avoid the potential reduction in systemic vascular resistance that
often occurs when general anesthesia is administered to a chronically hypertensive
patient’s. However, considering her increased risk for aspiration (history of GERD
and diabetes), and the potentially detrimental affects of tachycardia in the setting of
mitral valve stenosis, I would ensure adequate analgesia, to avoid tachycardia and
minimize sedative requirements (increasing levels of sedation lead to increased risk
of impaired airway reflexes).
While catheter ablations are commonly performed under MAC or deep sedation, there
are certain advantages to performing the procedure under general anesthesia, such as
patient comfort during a long procedure, better blunting of sympathetic stimulation
(avoiding tachycardia is very important in patients with mitral valve stenosis ), control
of the airway and ventilation (may help to avoid hypercarbia, which can increase
pulmonary vascular resistance), and the option for immediate surgical intervention
should a complication occur.
What’s the deal with beta blockers in people who are on calcium channel blockers?
While ~-blockers are often used for rate control in atrial fibrillation,
they should not be combined with calcium channel blockers due to the risk for severe
cardiac depression. This would be of particular concern in this patient with signs of
right heart strain (EKG and tricuspid regurgitation).
During
electrophysiologic mapping the blood pressure suddenly drops to 44/21. What
do you think is the cause? What would you do?
Acute hemodynamic instability during electrophysiologic mapping is
usually the result of a cardiac arrhythmia such as ventricular tachycardia or
fibrillation. However, I would also consider other potential causes related to this
procedure and the patient’s comorbidities, such as myocardial ischemia, acute heart
failure, cardiac tamponade, cardiac rupture, undiagnosed hemorrhage, pulmonary
embolism, and acute air embolism. Moreover, if a central line were placed, I would
consider the possibility of tension pneumothorax.
In managing this situation, I would immediately inform the surgeon, discontinue any
volatile agent, evaluate the EKG, palpate the pulse, auscultate the chest, ensure
adequate oxygenation, place the patient in the trendelenburg position (to increase
preload), and administer fluids, vasopressors, and inotropes as indicated. While
treating her, I would keep in mind that arrhythmia-induced or reflex tachycardia
limits the ventricular filling time in patients with mitral valve stenosis, potentially
exacerbating her condition. If my initial interventions were ineffective, I would
consider obtaining an echocardiogram and chest X-ray to identify the problem and
guide therapy (a pulmonary artery catheter would potentially prove helpful, but would
be associated with the risks previously discussed).
Despite your interventions the blood pressure does not improve. The surgeon
performs fluoroscopy, which shows the ablation catheter curled in the left chest.
What would you do? (pt had low bp to systolic of 44)
Recognizing that this is consistent with cardiac rupture, I would: (1)
ask the cardiologist to inform the operating room of the emergent case and consult a
cardiovascular surgeon for emergency repair; (2) begin fluid resuscitation; (3) prepare
for massive blood transfusion (i.e. initiate protocol, ensure blood typing, adequate
intravenous access); (4) administer vasopressors as indicated; and (5) place an arterial
line and TEE to guide therapy. If there were evidence of cardiac tamponade
(diastolic collapse of the right atrium, right ventricle, and/or left ventricle, as
determined by TEE, is the most sensitive and specific sign of cardiac tamponade), I
would ask the surgeon to decompress the pericardium.
PADS Criteria
