26: Cardiac Flashcards
The internal mammary artery (also known as internal thoracic artery) collateralizes with which artery?
Superior epigastric artery
[Wikipedia: In human anatomy, superior epigastric artery refers to a blood vessel that carries oxygenated blood and arises from the internal thoracic artery (referred to as the internal mammary artery in the accompanying diagram). It anastomoses with the inferior epigastric artery at the umbilicus and supplies the anterior part of the abdominal wall and some of the diaphragm.]
What is the usual timing of repair for a large (shunt greater than 2.5) ventricular septal defect?
1 year of age
[Most common reason for earlier repair is failure to thrive]
[UpToDate: Unless surgery is performed in the 1st year of life, there is increasing likelihood that elevated PVR will become fixed, preventing successful repair. Irreversible pulmonary vascular disease develops earlier in children with trisomy 21; large VSDs in such children should be repaired by 3 to 4 months of age.]
Which direction is blood shunted in patent ductus arteriosus?
Left to right
[UpToDate: In the fetus, constriction of the pulmonary arteries leads to high vascular resistance, whereas the fetal systemic vascular resistance is low as a large proportion of the systemic circulation (about 40%) flows into the placenta, which has a very low vascular resistance. As a result, the majority of the blood flow exiting from the right ventricle bypasses the pulmonary arteries in a right-to-left shunt across the ductus arteriosus (DA) into the descending aorta and on to the placenta. In the fetus, because of the large right-to-left shunting of blood, the ductus is a large vessel with a diameter similar to that of the descending aorta.
With the onset of respiration after delivery, the lungs expand and the systemic oxygen saturation rises, resulting in pulmonary vasodilatation and a drop in pulmonary vascular resistance. At the same time, systemic resistance rises with placental removal. These factors lead to a sudden reversal of blood flow in the DA from right-to-left to left-to-right shunting.]
What medication can be used to treat symptoms of tetralogy of fallot?
Beta-blockers
[UpToDate: Hypercyanotic (or “tet”) spells present as periods of profound cyanosis that occur because of episodes of almost total RVOT obstruction. They typically arise when an infant becomes agitated or in older, uncorrected children after vigorous exercise.
The management of hypercyanotic “tet” spells requires a rapid and aggressive step-wise treatment. Escalation to the next step is dependent on the patient’s response.
- Treatment starts with placement of the patient in a knee-chest position to increase systemic vascular resistance, which promotes movement of blood from the right ventricle into the pulmonary circulation rather than the aorta.
- Oxygen should be administered as it acts as a pulmonary vasodilator and a systemic vasoconstrictor.
- If these fail, they are followed by intravenous therapy of morphine (0.1 mg/kg per dose) and an intravenous fluid bolus (10 to 20 cc/kg normal saline). The mechanism of action of morphine is unclear, while fluids improve right ventricle (RV) filling and pulmonary flow. The role of bicarbonate therapy to treat an associated lactic acidosis is uncertain.
- If the above measures fail, intravenous beta blockers (eg, propranolol, 0.1 mg/kg per dose, or esmolol, 0.1 mg/kg per dose) can be administered. The presumed mechanism of benefit is relaxation of the RVOT with improved pulmonary blood flow. If this is insufficient, systemic afterload can be increased with intravenous phenylephrine (5 to 20 mcg/kg per dose), which, as with assumption of the knee-chest position, promotes right ventricular flow into the pulmonary circulation rather than the aorta.
- If all of these measures fail, emergency complete surgical repair or an emergency aorticopulmonary shunt (ie, Blalock-Taussig shunt) is necessary.]
Superior vena cava (SVC) syndrome is most commonly secondary to what?
Lung cancer invading the SVC
[These tumors are unresectable since the tumor has invaded the mediastinum]
[UpToDate: In the preantibiotic era, syphilitic thoracic aortic aneurysms, fibrosing mediastinitis, and other complications of untreated infection were frequent causes of superior vena cava (SVC) syndrome. Subsequently, malignancy became the most common cause, accounting for 90% of cases by the 1980s. More recently, the incidence of SVC syndrome due to thrombosis has risen, largely because of increased use of intravascular devices, such as catheters and pacemakers. Benign causes now account for 20% to 40% of cases of SVC syndrome.
An intrathoracic malignancy is responsible for 60% to 85% of cases of SVC syndrome, and SVC obstruction is the presenting symptom of a previously undiagnosed tumor in up to 60% of these cases. Non-small cell lung cancer (NSCLC) is the most common malignant cause of SVC syndrome, accounting for 50% of all cases, followed by small cell lung cancer (SCLC, 25% of all cases) and non-Hodgkin lymphoma (NHL, 10% of cases). Together, lung cancer and NHL are responsible for approximately 95% of cases of SVC syndrome that are caused by malignancy.]
What is the most common congenital heart defect that results in cyanosis?
Tetralogy of fallot
[UpToDate: The prevalence of TOF in the United States is approximately 4 to 5 per 10,000 live births. This defect accounts for about 7% to 10% of cases of congenital heart disease and is one of the most common congenital heart lesions requiring intervention in the first year of life. TOF occurs equally in males and females.]
What is the most common congenital heart defect?
Ventricular septal defect
[Causes left to right shunt]
[UpToDate: Ventricular septal defect (VSD) is one of the most common congenital heart lesions (second only to bicuspid aortic valve). It occurs in almost 50% of all patients with congenital heart disease (CHD), with a reported prevalence of 4 per 1000 live births.]
What is often used as the first procedure in treating mitral stenosis?
Balloon commissurotomy to open the valve
[Not as invasive]
[UpToDate: When interventions are warranted in patients with rheumatic mitral stenosis (MS), percutaneous mitral balloon valvotomy (PMBV) is preferred to surgery unless there are contraindications to PMBV.
Surgery is usually preferred in patients with congenital MS, since the anatomy is complex, the utility of PMBV may be limited, and catheterization procedures are potentially dangerous.
PMBV and surgical commissurotomy can be repeated as long as the valve morphology remains favorable.
Closed commissurotomy is associated with worse long-term outcomes compared to PMBV and is now rarely performed in developed countries. It is still performed in some developing nations where cost and lack of balloon valvotomy capability are continuing problems.
Open commissurotomy is an appropriate choice in patients with suitable valve morphology who are not candidates for PMBV due to valve deformity or calcification, left atrial thrombus, or significant mitral regurgitation.
Mitral valve replacement is indicated for patients with moderate to severe mitral stenosis (mitral valve area ≤1.5 cm2) who have NYHA class III or IV symptoms, who are not at high risk for surgery, and have a mitral valve not amenable to either PMBV or open commissurotomy.]
What is the most common cause of death in the United States?
Coronary artery disease
What are the risk factors for postoperative mediastinitis?
Obesity, use of bilateral internal mammary arteries, diabetes
[UpToDate: The following risk factors for postoperative sternal wound infection have been described:
In adults:
- Diabetes or perioperative hyperglycemia
- Obesity
- Peripheral artery disease
- Tobacco use
- Prior cardiac surgery
- Mobilization of the internal mammary arteries
- Prolonged surgical procedure (greater than five hours)
- Return to the operating room within four days postoperatively (eg, control bleeding)
- Prolonged postoperative intensive care
In children:
- Age <1 year
- Male gender
The incidence of postoperative mediastinitis ranges from 0.4% to 5%, with the incidence in most centers being between 1% and 2%. However, the risk may be considerably higher in certain subsets of patients. As an example, the rates have ranged from 2.5% to 7.5% in patients undergoing heart transplantation, and may be higher if cardiac assist devices are used.]
What medications can be used to treat symptoms of ventricular septal defect and atrial septal defect?
Diuretics and digoxin
Which blood vessels travel in the umbilical cord?
2 umbilical arteries and 1 umbilical vein
What is the most common malignant tumor of the heart?
Angiosarcoma
[UpToDate: Malignant tumors constitute approximately 15% of primary cardiac tumors. Sarcomas are the most common, although other tumor types have been reported. Of sarcomas, 40% are angiosarcomas, and 10% are spindle sarcomas
Angiosarcomas are composed of malignant cells that form vascular channels. The pathology of angiosarcomas may overlap with Kaposi sarcoma, which can also involve the myocardium. Angiosarcomas arise predominantly in the right atrium. Epithelioid hemangioendothelioma, another sarcoma of vascular origin, has also been reported.]
Which kind of atrial septal defect can have mitral valve and tricuspid valve problems?
Ostium primum (or atrioventricular canal defects or endocardial cushion defects)
[UpToDate: The primum type ASD develops if the septum primum does not fuse with the endocardial cushions, leaving a defect at the base of the interatrial septum that is usually large. This type of defect accounts for 15% to 20% of ASDs. Primum ASDs are usually not isolated, typically being associated with atrioventricular (AV) canal defects that include anomalies of the AV valves and defects of the ventricular septum.]
What is the usual timing of repair for a medium (shunt 2-2.5) ventricular septal defect?
5 years of age
[Most common reason for earlier repair is failure to thrive]
[UpToDate: Though moderate ventricular septal defects can be pressure restricted, meaning pulmonary artery (PA) and RV pressures are <50% of systemic arterial systolic pressures, the degree of left-to-right shunt may be significant enough to cause congestive symptoms. Most cases with moderate-size VSDs respond to medical therapy, and pulmonary vascular resistance (PVR) usually does not increase in these patients. As a result, surgical or catheter-based intervention is often not required. The risk of development of irreversible pulmonary vascular obstructive disease increases when pulmonary arterial pressures are greater than 50% of systemic pressures, a level which should prompt closure of the defect.
Other children with moderate VSDs and a persistent left-to-right shunt may remain hemodynamically and clinically stable, or improve for several years despite increased left atrial and ventricular volume. This observation was illustrated by a long-term follow-up study (mean time of follow-up 7.8 years) of 33 unoperated children with moderate-size, restrictive VSDs with severe LV dilation but no evidence of cardiac failure or pulmonary arterial hypertension. At follow-up, these patients had a spontaneous reduction in LV dilation measured by echocardiography (decrease of mean LV end-diastolic dimension z score from 3 to 1.2) suggesting smaller LV volumes due to reduced left-to-right shunt.]
What is the most common kind of atrial septal defect?
Ostium secundum (80%)
[Centrally located]
[UpToDate: Secundum defects account for approximately 70% of all ASDs, and occur twice as often in females as in males. Familial recurrent rate has been estimated to be about 7% to 10%. A comprehensive literature review reported a median incidence of 564 per million live births. However, the true incidence of secundum atrial septal defect may be substantially higher because many ASDs are commonly undiagnosed in infancy and childhood, and spontaneously resolve.
Secundum ASDs are typically located within the fossa ovalis (remnant of the foramen ovale in the right atrium). This type of ASD can result from arrested growth of the secundum septum or excessive absorption of the primum septum. Multiple defects can be seen if the floor of the fossa ovalis is fenestrated. The defects vary greatly in size, from less than 3 mm to greater than 20 mm.
Secundum ASDs may be associated with or continuous with other ASDs, such as a sinus venosus defect or a primum defect. Some patients with secundum ASD have functional mitral valve prolapse, perhaps related to a change in the left ventricular geometry associated with right ventricular volume overload.]
What are the 3 cardinal symptoms of aortic stenosis?
- Dyspnea on exertion (5-year mean survival)
- Angina (4-year mean survival)
- Syncope (3-year mean survival)
[syncope is the worst of the cardinal symptoms]
[UpToDate: The classic clinical manifestations of aortic stenosis (AS) are heart failure (HF), syncope, and angina. However, these “classic” manifestations reflect end-stage disease. Now, with earlier diagnosis by echocardiography and prospective followup of patients, the following are the most common presenting symptoms:
- Dyspnea on exertion or decreased exercise tolerance
- Exertional dizziness (presyncope) or syncope
- Exertional angina
These three “early symptoms” are nonspecific. Care must be taken in attributing these symptoms to AS since most patients with these symptoms do not have AS.]
What is the best conduit for coronary artery bypass grafting?
Internal mammary artery (also known as internal thoracic artery)
[UpToDate: Patency rates for arterial grafts at 10 years are as high as 98% and arterial graft patency is associated with long-term survival. As this high rate far exceeds that for vein grafts, an attempt is made to place at least one arterial graft in every patient who undergoes coronary artery bypass graft surgery (CABG).]
Severe mitral regurgitation with hypotension and pulmonary edema occuring 3-7 days after myocardial infarction is suspicous for what?
Papillary muscle rupture
[UpToDate: Papillary muscle rupture is a life-threatening complication of acute MI that accounts for approximately 5% of deaths in these patients. It usually occurs 2 to 7 days after the infarct. The rupture may be partial (occurring at one of the muscle heads) or complete.
Because of differences in blood supply, rupture of the posteromedial papillary muscle occurs 6 to 12 times more frequently than rupture of the anterolateral papillary muscle. The posteromedial papillary muscle is supplied with blood from the posterior descending artery, while the anterolateral papillary muscle has a dual blood supply from the left anterior descending and left circumflex arteries.
The clinical manifestations of papillary muscle rupture include the acute onset of hypotension and pulmonary edema with a hyperactive precordium and a mid-, late-, or holosystolic murmur that may have widespread radiation. Although the murmur may be loud, a thrill is generally not present. Furthermore, as noted above, many patients have no or only a soft murmur.]
Atrial septal defects are usually symptomatic when the shunt is greater than what?
2:1
[This means for every 1 volume equivalent passing from the left atrium to the left ventricle, 2 volume equivalents pass from the left atrium to the right atrium]
Hypotension and a pansystolic murmur occuring 3-7 days after myocardial infarction is suspicous for what?
Ventricular septal rupture
[UpToDate: The frequency of septal rupture has been reported to be about half that of free wall rupture. It typically occurs 3 to 5 days after an acute myocardial infarction (MI). It may, however, develop within the first 24 hours or as late as 2 weeks.
An increased risk of septal rupture may be observed in patients with single-vessel disease (especially the left anterior descending artery), extensive myocardial damage, and poor septal collateral circulation. Septal rupture may also be seen in patients with multivessel coronary artery disease and there is a higher prevalence in first infarctions.
Due to the nature of the septal blood supply, patients with an MI due to occlusion of a “wraparound” left anterior descending (LAD) artery appear to have an elevated risk of septal rupture. In most individuals, the inferior one-third of the septum is supplied by the right coronary artery. In some individuals, however, the LAD extends beyond the left ventricular apex, wrapping around to supply the distal inferior wall and inferior septum.
In patients with a “wraparound” LAD, an anterior MI due to LAD occlusion can result in more extensive septal infarction and reduced collateral supply to the septum, producing an increased risk of septal rupture and ST elevation in the inferior leads. In contrast, patients with a high lateral wall MI are more likely to have reciprocal ST depression in the inferior leads, while other patients have no inferior ST segment changes.
Based upon these observations, ECG evidence of infarction with a wraparound LAD (inferior ST elevation during a large anterior MI) may identify patients at high risk. In a report comparing 21 patients with an anterior MI and septal rupture to 275 similar patients without septal rupture, the patients with septal rupture were much more likely to have ST segment elevations (43% vs 4%) and Q waves (44% vs 4%) in all three inferior leads (II, III, and aVF).]
What is the treatment for superior vena cava (SVC) syndrome secondary to cancer invading the SVC?
Emergent XRT
[These tumors are unresectable since the tumor has invaded the mediastinum]
[UpToDate: In the past, SVC syndrome due to malignant disease was considered a potentially life-threatening medical emergency requiring immediate radiation therapy (RT) as the quickest way to relieve the obstruction. Emergency RT is no longer considered necessary for most patients for several reasons:
- Symptomatic obstruction is often a prolonged process, developing over a period of weeks or longer prior to clinical presentation. The duration of symptoms has no influence on treatment outcomes. Deferring therapy until a full diagnostic work-up has been completed does not pose a hazard for most patients, provided the evaluation is efficient and the patient is clinically stable. This was illustrated in a review of 107 cases of SVC syndrome in which no serious complication resulted from the SVC obstruction itself or investigative procedures leading to the diagnosis, despite a prolonged period between the onset of symptoms and the initiation of therapy in some cases.
- RT prior to biopsy may obscure the histologic diagnosis. As an example, in one study of 19 patients with symptomatic mediastinal masses who received emergency RT, a histologic diagnosis could not be established in eight (42%) from a biopsy obtained after such treatment.
Current management guidelines stress the importance of accurate histologic diagnosis prior to starting therapy and the upfront use of endovenous stents in severely symptomatic patients to provide more rapid relief than can be achieved using RT.
Important exceptions to this general approach are patients who present with stridor due to central airway obstruction or severe laryngeal edema, and those with coma from cerebral edema. These situations represent a true medical emergency, and these patients require immediate treatment (stent placement and RT) to decrease the risk of sudden respiratory failure and death.]
What is the treatment for post-pericardiotomy syndrome?
NSAIDs and steroids
[UpToDate: For patients who develop post-cardiac injury syndrome, first-line treatment consists of nonsteroidal anti-inflammatory drugs (NSAIDs), usually in combination with colchicine, though there are no randomized controlled trials of different dosing regimens. Either aspirin or a different NSAID (eg, ibuprofen, naproxen, etc) may be tried as initial therapy if there are no contraindications. Colchicine may also be effective in the treatment of post-cardiac injury syndrome, although there are limited data in this setting.
In contrast to colchicine, prophylactic glucocorticoid therapy in patients undergoing cardiac surgery appears to have no beneficial effect on post-cardiac injury syndrome. In a single-center post-hoc analysis of 822 patients from the DECS trial who underwent valvular surgery and received a one-time intraoperative dose of 1 mg/kg of dexamethasone (421 patients) or placebo (401 patients), there was no significant difference in the development of postpericardiotomy syndrome (13.5% vs 15.5% with placebo; RR 0.88; 95% CI 0.63-1.22); moreover, the incidence of a complicated postpericardiotomy syndrome (defined as the need to drain a pericardial or pleural effusion, or rehospitalization for a recurrence) was similar (3.8% vs 3.2%, respectively; RR 1.17; 95% CI 0.57-2.41).]
Following a cardiac procedure, how much mediastinal bleeding is criteria for re-exploration?
Greater than 500cc in 1 hour or greater than 250cc/hr for 4 straight hours
What are the 4 best indications for coronary artery bypass grafting?
- Greater than 50% stenosis of left main or greater than 70% stenosis for all others
- 3-vessel disease (Left anterior descending, circumflex, and right coronary artery)
- 2-vessel disease involving the left anterior descending
- Lesions not amenable to stenting
[UpToDate: The decision to proceed with revascularization with either coronary artery bypass graft surgery or percutaneous coronary intervention (PCI), as opposed to continuing medical therapy, is made in three groups of stable patients:
Patients with activity-limiting symptoms despite maximum medical therapy.
Active patients who want PCI for improved quality of life compared to medical therapy, such as those who are not tolerating medical therapy well, or who want to increase their activity level.
Patients with anatomy for which revascularization has a proven survival benefit such as significant left main coronary artery disease (greater than 50% luminal narrowing) or multivessel coronary artery disease with a reduction of left ventricular ejection fraction and a large area of potentially ischemic myocardium.]
What is the most common benign tumor of the heart?
Myxoma
[75% in the left atrium]
[UpToDate: Myxomas are the most common primary cardiac neoplasm. Histologically, these tumors are composed of scattered cells within a mucopolysaccharide stroma. The cells originate from a multipotent mesenchyme that is capable of neural and endothelial differentiation. Myxomas produce vascular endothelial growth factor (VEGF), which probably contributes to the induction of angiogenesis and the early stages of tumor growth.
Macroscopically, typical myxomas are pedunculated and gelatinous in consistency; the surface may be smooth, villous, or friable. Tumors vary widely in size, ranging from 1 to 15 cm in diameter, and weigh between 15 and 180 g. About 35% of myxomas are friable or villous, and these tend to present with emboli. Larger tumors are more likely to have a smooth surface and to be associated with cardiovascular symptoms.]
The internal mammary artery (also known as internal thoracic artery) is a branch off which artery?
Subclavian
What is the 20-year patency of coronary artery bypass grafting with the internal mammary artery (also known as internal thoracic artery) when placed to the left anterior descending?
Greater than 95%
[UpToDate: Patency rates for arterial grafts at 10 years are as high as 98% and arterial graft patency is associated with long-term survival. As this high rate far exceeds that for vein grafts, an attempt is made to place at least one arterial graft in every patient who undergoes coronary artery bypass graft surgery (CABG).]
What is the most common site of native valve endocarditis?
Mitral valve
[UpToDate: Mitral valve disease, such as mitral valve prolapse (usually with coexistent mitral regurgitation) and/or mitral annulus calcification, is a risk factor for IE. Two reports of IE noted mitral valve prolapse was the underlying cardiac lesion in 22% and 29% of cases. The risk of IE in patients with mitral valve prolapse and associated regurgitation is estimated to be five to eight times higher than that in patients with a normal mitral valve. In addition, mitral valve prolapse has been associated with viridans group streptococcal IE. However, mitral valve prolapse without mitral insufficiency is a more common abnormality that is associated with only a small risk of endocarditis.
Aortic valve disease (sclerosis, stenosis, and/or regurgitation) occurs in 12% to 30% of IE cases.]
What does squatting do to systemic vascular resistance?
Increases it
[UpToDate: Squatting from a standing position is associated with a simultaneous increase in venous return (preload) and systemic vascular resistance (afterload) and a rise in arterial pressure. This causes changes in the following murmurs:
Increased intensity of the murmur of mitral regurgitation due to the rise in afterload, which favors the movement of blood in the left ventricle across the regurgitant mitral valve into the left atrium rather than entering the systemic circulation across the aortic valve.
In patients with mitral valve prolapse there is a delay in the onset of the click and a shortening of the late systolic murmur. These changes reflect the delay in prolapse induced by the increase in preload. However, as mitral regurgitation becomes more severe, the murmur may increase in intensity with squatting because of the increase in afterload.
Increase in the magnitude of the left-to-right shunt in ventricular septal defect associated with an increased intensity of the systolic murmur.
In patients with tetralogy of Fallot, the net effect of squatting is usually an increase in pulmonary flow, which is associated with increased intensity of the pulmonary ejection systolic murmur.
Intensity of the diastolic murmur of aortic regurgitation increases due to augmented regurgitation; intensity of the Austin-Flint murmur also may increase.
In hypertrophic cardiomyopathy, intensity of the ejection systolic murmur promptly declines because of an increased left ventricular volume and arterial pressure, which increase the effective orifice size of the outflow tract; the carotid pulse upstroke remains sharp, and the volume may increase.
Intensity of the murmur of valvular aortic stenosis shows variable changes, depending upon the type of hemodynamic response; a significant increase in systemic vascular resistance is associated with a decreased intensity of the murmur, an increased left ventricular volume with increased intensity of the murmur. There is usually no change or a decrease in the intensity of a benign flow murmur.]
What is the most common heart valve lesion?
Aortic stenosis
[Calcification produces stenosis]
[UpToDate: The relative frequency of the causes of aortic stenosis (AS) varies geographically. Worldwide, rheumatic valve disease is most common and mitral valve involvement invariably accompanies rheumatic aortic valve disease. In North America and Europe, aortic valve disease is primarily due to calcific disease of a native trileaflet valve or a congenitally bicuspid valve.]
What does the surgical repair of tetralogy of fallot entail?
- Right ventricular outflow tract obstruction removal
- Right ventricular outflow tract enlargement
- Ventricular septal defect repair
Which kind of atrial septal defect is frequent in Down’s syndrome?
Ostium primum
[UpToDate: The primum type ASD develops if the septum primum does not fuse with the endocardial cushions, leaving a defect at the base of the interatrial septum that is usually large. This type of defect accounts for 15% to 20% of ASDs. Primum ASDs are usually not isolated, typically being associated with atrioventricular (AV) canal defects that include anomalies of the AV valves and defects of the ventricular septum.]
What is superior vena cava (SVC) syndrome?
Swelling of the upper extremities and face, most commonly secondary to lung cancer invading the SVC
[UpToDate: Superior vena cava (SVC) syndrome results from any condition that leads to obstruction of blood flow through the SVC. Obstruction can be caused by invasion or external compression of the SVC by an adjacent pathologic process involving the right lung, lymph nodes, and other mediastinal structures, or by thrombosis of blood within the SVC. In some cases, both external compression and thrombosis coexist.
Obstruction of the superior vena cava (SVC) can be caused by invasion or external compression by adjacent pathologic processes involving the right lung, lymph nodes, or other mediastinal structures, or by thrombosis of blood within the SVC. As the flow of blood within the SVC becomes obstructed, venous collaterals form, establishing alternative pathways for the return of venous blood to the right atrium. Collateral veins may arise from the azygos, internal mammary, lateral thoracic, paraspinous, and esophageal venous systems.
The venous collaterals dilate over several weeks. As a result, upper body venous pressure is markedly elevated initially but decreases over time. However, even when well-developed collateral drainage patterns are present, central venous pressures remain elevated, producing the characteristic signs and symptoms of SVC syndrome.
The rapidity of onset of symptoms and signs from SVC obstruction depends upon the rate at which complete obstruction of the SVC occurs in relation to the recruitment of venous collaterals. Patients with malignant disease may develop symptoms of SVC syndrome within weeks to months because rapid tumor growth does not allow adequate time to develop collateral flow. In contrast, fibrosing mediastinitis due to an infection, such as histoplasmosis, may not become symptomatic for years.
The interstitial edema of the head and neck is visually striking but generally of little clinical consequence. However, edema may narrow the lumen of the nasal passages and larynx, potentially compromising the function of the larynx or pharynx, and causing dyspnea, stridor, cough, hoarseness, and dysphagia. In addition, cerebral edema can also occur and lead to cerebral ischemia, herniation, and possibly death.]
Do bioprosthetic valves require anticoagulation?
No
[UpToDate:A major advantage of bioprosthetic valves is a low long-term rate of thromboembolism in the absence of risk factors such as atrial fibrillation, a low left ventricular ejection fraction, or a large left atrium. The reported rate of thromboembolic stroke has ranged from 0.2% to 3.3% per year in different studies, but is only 0.7% per year in patients in sinus rhythm. The risk is greater with valves in the mitral compared with aortic position, where the risk may be as low as 0.2% in patients in sinus rhythm.
The following recommendations are generally consistent with the 2014 AHA/ACC valve guidelines:
- For patients with bioprosthetic aortic or mitral valves, we suggest aspirin 75 to 100 mg per day.
- For patients with a bioprosthetic mitral or tricuspid valve replacement, we suggest anticoagulation with a vitamin K antagonist (VKA) for the first 3 months to achieve an INR of 2.5.
- For patients with a surgical bioprosthetic aortic valve replacement, we suggest anticoagulation with a VKA for the first 3 months to achieve an INR of 2.5 (this is a weaker recommendation than that for patients who have undergone mitral valve surgery in the 2014 AHA/ACC valve guidelines).
- For patients with bioprosthetic valves who have an indication for intermediate (3 months) or indefinite anticoagulation (eg, concurrent atrial fibrillation with thromboembolic risk factors), we suggest use of early bridging anticoagulation as soon as the risk of postoperative bleeding is considered acceptable. We suggest treatment with UFH or LMWH until the INR is at therapeutic levels for two consecutive days.]
Which patients are more appropriate candidates for a bioprosthetic valve
Patients who want pregnancy, have contraindication to anticoagulation, are >65 years and unlikely to require another valve in their lifetime, or have frequent falls
What does a ductus venosus connect?
Portal vein and the inferior vena cava
[shunts blood away from the liver in utero]
Which direction is blood shunted in tetralogy of fallot?
Right to left
The left main coronary artery branches into what?
The left anterior descending and circumflex arteries
What are the 4 anatomic anomolies in tetralogy of fallot?
- Ventricular septal defect
- Pulmonic stenosis
- Overriding aorta
- Right ventricular hypertrophy
[causes right to left shunt]
What is the treatment for ventricular septal rupture?
Intra-aortic balloon pump to temporize, patch over septum
[UpToDate:The timing of surgical repair in patients with post-MI ventricular septal rupture is controversial. Early retrospective studies noted lower operative mortality rates in patients who underwent surgery more than 6 weeks after infarction than in those who underwent earlier operation. However, these observations reflected selection bias, in which patients with relatively well-preserved left ventricular function and smaller defects survived to become low risk surgical candidates.
The optimal approach varies with the clinical presentation. In patients with cardiogenic shock, death is inevitable in the absence of urgent surgical intervention. Stabilization is attempted with vasodilators (which reduce afterload, thereby decreasing left ventricular pressure and the left to right shunt), inotropic agents (which may increase the cardiac output), diuretics, and intraaortic balloon pump counterpulsation (which has actions similar to vasodilators).
This is followed by cardiac catheterization to define the coronary anatomy and then surgical repair. Operative mortality is high in this setting, but the late results in survivors are excellent.]
What does a ductus arteriosus connect?
Descending aorta to left pulmonary artery
[shunts blood away from lungs in utero]
Mitral stenosis is rare and most commonly occurs secondary to what?
Rheumatic fever
[UpToDate: Rheumatic heart disease (RHD) is the most common cause of mitral stenosis (MS); other causes are much less frequent. However, only 50% to 70% of patients with MS report a history of rheumatic fever. RHD remains a major public health problem in developing countries. Rheumatic MS has become less common in developed countries given marked reductions in the incidence of rheumatic fever. Occasional outbreaks of rheumatic fever in the United States appear to be the result of either increased virulence of a streptococcal strain or enhanced immigration from areas where RHD is prevalent. Involvement of the mitral valve is present in approximately 90% of individuals with RHD. In many populations, RHD is more common in females than in men. Rheumatic MS is a continuously progressive lifelong disease.]
A sudden step-up in oxygen content between the right atrium and pulmonary artery in the setting of a myocardial infarction is suspicious of what?
Ventricular septal rupture
[Due to left to right shunt]
[UpToDate: Patients with a ruptured septum usually present with the precipitous onset of hemodynamic compromise characterized by hypotension, biventricular failure (often predominantly right-sided failure), and a new murmur. The murmur is harsh, loud, and holosystolic, and is heard best at the lower left and usually right sternal borders, with occasionally widespread radiation. In some cases, the murmur is heard best at the apex and may be mistaken for acute mitral regurgitation. A thrill can be detected in up to 50% of patients; right ventricular lift and a hyperdynamic precordium may also be noted.
Among patients who are not effectively reperfused, septal rupture is often associated (15 of 17 in one series) with persistent ST segment elevation for more than 72 hours. The risk of septal rupture is increased in patients with right ventricular infarction.]
What test is most appropriate to diagnose ventricular septal rupture?
Echo
[UpToDate: Confirmation of the diagnosis usually requires insertion of a pulmonary artery balloon catheter to document the left-to-right shunt. Occasionally, giant pulmonary capillary wedge pressure V waves occur because of severe volume overload in the setting of reduced atrial and ventricular compliance.
The defect can also be diagnosed by two-dimensional transthoracic echocardiography with color flow Doppler imaging. One study, for example, evaluated 43 patients with a post-MI ventricular septal defect. Two-dimensional echocardiography alone visualized the defect in only 17 (40%) of the patients. However, the addition of Doppler color flow mapping demonstrated both an area of turbulent transseptal flow and a diagnostic systolic flow disturbance within the right ventricular in all 43 patients. Transesophageal echocardiography may occasionally be necessary to delineate the complete extent of the abnormality.]
What test is most appropriate to diagnose papillary muscle rupture?
echocardiogram
UpToDate: The diagnosis of papillary muscle rupture or severe dysfunction is suggested by the combination of hemodynamic compromise and a new systolic murmur in the setting of an acute myocardial infarction. An echocardiographic study evaluating 50 such patients found that 43 had a ventricular septal defect (VSD) and seven had papillary muscle rupture or severe dysfunction.
The diagnosis of papillary muscle disease after MI is typically confirmed by echocardiography (with color flow Doppler) and cardiac catheterization is performed to define the coronary anatomy. Two-dimensional transthoracic echocardiography usually demonstrates a flail segment of the mitral valve, and a severed papillary muscle or chordae can frequently be seen moving freely within the left ventricular cavity. In some cases, however, transthoracic echocardiography is not informative and transesophageal echocardiography is required to establish the diagnosis; this is most likely to occur in those patients in whom the ruptured head does not prolapse into the left atrium (which may occur in up to 35% of cases). Left ventricular function is usually hyperdynamic as a result of ventricular contraction against the low impedance left atrium.]
What percent of cardiac patients have saphenous vein graft patency after 5 years?
80%
[UpToDate: Late occlusion sometime after the first 12 to 18 months occurs when the areas of intimal hyperplasia develop lipid deposition and finally an atherosclerotic-like plaque. From the end of year 1 to year 6, SVGs obstruct at the rate of approximately 2% per year; the subsequent closure rate rises to 4% to 5% per year.]
Why does squatting help individuals with right to left shunts?
It increases systemic vascular resistance and thus decreases Right to left shunting of blood
[UpToDate: Squatting from a standing position is associated with a simultaneous increase in venous return (preload) and systemic vascular resistance (afterload) and a rise in arterial pressure. This causes changes in the following murmurs:
Increased intensity of the murmur of mitral regurgitation due to the rise in afterload, which favors the movement of blood in the left ventricle across the regurgitant mitral valve into the left atrium rather than entering the systemic circulation across the aortic valve.
In patients with mitral valve prolapse there is a delay in the onset of the click and a shortening of the late systolic murmur. These changes reflect the delay in prolapse induced by the increase in preload. However, as mitral regurgitation becomes more severe, the murmur may increase in intensity with squatting because of the increase in afterload.
Increase in the magnitude of the left-to-right shunt in ventricular septal defect associated with an increased intensity of the systolic murmur.
In patients with tetralogy of Fallot, the net effect of squatting is usually an increase in pulmonary flow, which is associated with increased intensity of the pulmonary ejection systolic murmur.
Intensity of the diastolic murmur of aortic regurgitation increases due to augmented regurgitation; intensity of the Austin-Flint murmur also may increase.
In hypertrophic cardiomyopathy, intensity of the ejection systolic murmur promptly declines because of an increased left ventricular volume and arterial pressure, which increase the effective orifice size of the outflow tract; the carotid pulse upstroke remains sharp, and the volume may increase.
Intensity of the murmur of valvular aortic stenosis shows variable changes, depending upon the type of hemodynamic response; a significant increase in systemic vascular resistance is associated with a decreased intensity of the murmur, an increased left ventricular volume with increased intensity of the murmur. There is usually no change or a decrease in the intensity of a benign flow murmur.]
If a patent ductus arteriosus persists beyond the neonatal period, surgical repair is required from what approach?
Left thoracotomy
[UpToDate:In term infants and older children, the surgical approach is similar with a posterolateral thoracotomy. The incision is through the third left intercostal space in infants, and the fourth left intercostal space in older patients. Many surgeons prefer multiple ligations or division to minimize the risk of recurrent shunt.
Video-assisted thoracoscopic surgery (VATS) for PDA ligation can be a safe and effective procedure for PDA closure, and is less invasive than standard thoracotomy surgical closure. It involves isolation of the PDA using thoracoscopic techniques, and interruption of the PDA by placement of a surgical clip. Reported contraindications to VATS ligation include ductal diameter >9 mm, previous thoracotomy, ductal calcifications, active infection, and ductal aneurysm.]
What is the usual timing of repair for tetralogy of fallot?
3-6 months
[UpToDate: Currently, most patients with TOF undergo intracardiac repair as their initial intervention by 1 year of age, and over half before 6 months of age. However, palliative shunts may be needed for infants during a medically refractory hypercyanotic (“tet”) spell or for those with severe right ventricular outflow tract (RVOT) obstruction who may not be initially acceptable candidates for intracardiac repair due to prematurity, hypoplastic pulmonary arteries, or coronary artery anatomy.]
