Review Questions Flashcards
A 75 year old woman is noted to have a pulsatile mass in her abdomen on physical exam. She is not experiencing any pain. All laboratory values are within normal limits. Which of the following is the best option for further management?
A. Immediate transfer to surgery, followed by open repair
B. Biopsy
C. Obtain imaging, if <5.5 cm, close observation with repeat imaging
D. Obtain imaging to prepare for endovascular repair
A 75 year old woman is noted to have a pulsatile mass in her abdomen on physical exam. She is not experiencing any pain. All laboratory values are within normal limits. Which of the following is the best option for further management?
A. Immediate transfer to surgery, followed by open repair
B. Biopsy
C. Obtain imaging, if <5.5 cm, close observation with repeat imaging
D. Obtain imaging to prepare for endovascular repair
Explanation: The patient has AAA. Management of AAA is based on symptom and size: if the patient is symptomatic or there are concerns of rupture, surgical repair is the first option. Otherwise, the management is based on size of AAA. If the size is < 5.5cm, can be managed with repeat CT. If the size is > 5.5cm, go for surgical repair.
Learning objectives:
153a Understand the pathophysiology and treatment options for abdominal aortic aneurysms
Which of the following is NOT a risk factor for aortic aneurysm?
A. Marfan syndrome.
B. Hyperlipidimia and atherosclerosis.
C. Smoking
D. Diabetes
Which of the following is NOT a risk factor for aortic aneurysm?
A. Marfan syndrome.
B. Hyperlipidimia and atherosclerosis.
C. Smoking
D. Diabetes
Explanation: Aortic aneurysm is now believed to be caused by inflammatory cells releasing cytokines, leading to production of matrix metalloproteases that weakens the extracellular matrix in the blood vessel (degradation of collagen and elastin). This weakens the blood vessel structure and results in the formation of aneurysm. Marfan syndrome is a genetic disease of fibrillin mutation that results in absnormal connective tissue. Hyperlipidemia and associated atherosclerosis also results in weakening of the media of artery and formation of aneurysm. Other associated risk factors include smoking, old age, and male. African American descent and diabetes are actually protective against aneurysm.
Learning objectives
153a Explain the etiology of aneurysm formation and the pathophysiologic consequences of this disease
A 67 year old African American male presents with pain in his lower legs. This pain happens usually after about 4 blocks and goes away after he rests a bit. PMH is notable for smoking. Vitals: HR 80, RR 12, BP 151/82, Temp 97, Weight 240, Height 5’7. PE, PMH, SH, FH unremarkable. Which of the following is the most appropriate initial intervention for this patient?
A. Low dose aspirin daily
B. Clopidogrel
C. Revascularization
D. Lifestyle modification
E. Prophylatic toe amputation
A 67 year old African American male presents with pain in his lower legs. This pain happens usually after about 4 blocks and goes away after he rests a bit. PMH is notable for smoking. Vitals: HR 80, RR 12, BP 151/82, Temp 97, Weight 240, Height 5’7. PE, PMH, SH, FH unremarkable. Which of the following is the most appropriate initial intervention for this patient?
A. Low dose aspirin daily
B. Clopidogrel
C. Revascularization
D. Lifestyle modification
E. Prophylatic toe amputation
Explanation: The patient has claudication. The symptom is consistent with an early stage of the disease. The best option would be exercise, and lifestyle modification.
Learning objective:
153a Explain the natural history and pathophysiology of peripheral arterial disease
Atherosclerosis is associated with numerous well-known risk factors, such as age, smoking, diabetes, hyperlipidemia, and a family history of atherosclerosis. LDL-C is believed to be a key factor in the pathway through which hyperlipidemia causes atherosclerosis. What is the most likely first step in the pathogenesis of atherosclerosis caused by hyperlipidemia?
A. Endothelial dysfunction
B. Foam cell formation
C. LDL cholesterol oxidation
D. Monocyte activation
E. Plaque formation
Atherosclerosis is associated with numerous well-known risk factors, such as age, smoking, diabetes, hyperlipidemia, and a family history of atherosclerosis. LDL-C is believed to be a key factor in the pathway through which hyperlipidemia causes atherosclerosis. What is the most likely first step in the pathogenesis of atherosclerosis caused by hyperlipidemia?
A. Endothelial dysfunction
B. Foam cell formation
C. LDL cholesterol oxidation
D. Monocyte activation
E. Plaque formation
Explanation: Hyperlipidemia is a recognized risk factor for atherosclerosis. Current concepts describing the pathogenesis of this process suggest that
endothelial damage permits the movement of LDL-C into the subendothelial space. This LDL may then be modified (e.g. oxidized to oxLDL), which then may be taken up by macrophages, leading to the formation of foam cells, smooth muscle proliferation, and subsequent arterial plaques. The oxidation of LDL cholesterol increased monocytes/macrophage receptor affinity for the molecules and traps the lipid in the endothelial space. Macrophages that phagocytose these molecules become foam cells, which ten lead to other downstream effects of atherosclerosis such as calcification of occlusion of the vessel lumen. This in turn can lead to ischemia of various tissues, most notably the heart.
Learning objectives:
153a Explain the natural history and pathophysiology of peripheral arterial disease
129a Describe the natural history of atherosclerosis and understand how it manifests itself as MI, stroke, peripheral vascular disease, etc.
129a Describe the cellular and molecular etiology of atherosclerosis, and summarize how these cellular and molecular changes leads to the histopathologic changes seen.
132a Describe the role of endothelial dysfunction in leading to plaque rupture and erosion
Nitrates are often given as part of the management of angina. What is the primary mechanism by which nitrates work in the treatment of this condition?
A. Decrease in atrioventricular node conduction velocity
B. Decrease in heart rate and contractility
C. Increase in oxygen delivery to myocytes
D. Stimulate dilation of coronary arterioles
E. Stimulate venodilation
Nitrates are often given as part of the management of angina. What is the primary mechanism by which nitrates work in the treatment of this condition?
A. Decrease in atrioventricular node conduction velocity
B. Decrease in heart rate and contractility
C. Increase in oxygen delivery to myocytes
D. Stimulate dilation of coronary arterioles
E. Stimulate venodilation
Explanation: Nitrates are first line treatment in the management of angina. They act by stimulating the release of NO in smooth muscle, causing an increase in cGMP levels and subsequent smooth muscle relaxation, primarily in the venous system. Such venodilation causes a decrease in preload, which reduces left venticular wall stress and in turn minimizes myocardial oxygen consumption.
A. Mechanism of CCBs and adenosine
B. Beta blocker mechanism (also used to treat angina)
C. Nitrates act by stimulating venodilation to decrease preload and thereby reduce myocardial oxygen consumption. They do not act by increasing the oxygen supply to the myocardium. In the case of angina, cardiac vessels have depleted the dilation reserve.
D. Angina is caused by atherosclerotic stenosis within coronary arteries that limit blood flow through those vessels. Coronary arterioles in patients with flow limiting coronary stenosis are already dilated to maintain resting blood flow. Therefore, any vasodilating effects nitrates have on coronary arteries are negligible in the setting of already maximally dilated coronary arteries. Thus, stimulating the vasodilation of coronary arterioles is not the primary mechanism of nitrates in the treatment of angina.
Learning objective
131a Explain the role of medical therapy to reduce symptoms and improve quality of life
134a Predict the effects of anti-ischemic drugs on heart rate, blood pressure, myocardial inotropy, and coronary blood flow
Which of the following is not true regarding the coronary circulation?
A. During an event of angina, endocardium is the first part of the heart that is damaged.
B. Increased narrowing of coronary artery rapidly depletes the reserve vasodilation because of decreased coronary pressure after the stenotic area.
C. Most of the coronary resistance is controlled by the microvascular resistance, which in turn is controlled by metabolic factors and flow.
D. Atenolol would increase coronary circulation flow.
Which of the following is not true regarding the coronary circulation?
A. During an event of angina, endocardium is the first part of the heart that is damaged.
B. Increased narrowing of coronary artery rapidly depletes the reserve vasodilation because of decreased coronary pressure after the stenotic area.
C. Most of the coronary resistance is controlled by the microvascular resistance, which in turn is controlled by metabolic factors and flow.
D. Atenolol would increase coronary circulation flow.
Explanation: A. Because of higher compressive resistance, the vessel perfusing deeper myocardium are often at greater level of dilation and have lower dilatory reserve. This results in vulnerability when there is an increased demand of perfusion. B. Coronary artery stenosis would result in increased coronary pressure to maintain flow after the stenotic area. The majority of increased pressure is dissipated at the blockage (think about narrowing a hose to increase the water flow speed). C. In the myocardium, microvascular resistance plays a big role in determining the coronary resistance. This factor can be influenced by metabolism (the levels of adenosine) as well as the flow rate (which determines the production of vasodilator NO). D. Atenolol is a selective beta-1 antagonist would would have no effect on coronary circulation. The microvasculature of coronary vessel is mainly controlled by alpha and beta-2 adrenergic receptor. The blockade of former would lead to vasodilation and the blockade of latter would result in constriction. This is why selective beta-1 antagonist such as atenolol would be preferred.
Learning objective:
133a Explain coronary flow reserve and factors affecting its magnitude
133a Explain coronary atherosclerosis and factors determining the severity of a coronary artery stenosis
133a Explain the major factors governing coronary vascular resistance and coronary blood flow
133a Describe the normal balance between myocardial oxygen demand and coronary blood flow
134a Predict the effects of anti-ischemic drugs on heart rate, blood pressure, myocardial inotropy, and coronary blood flow
You are running a stress test. The patient has resting blood pressure 130/80 and heart rate of 75. The exercise goal is blood pressure 160/120 and heart rate of 150. Using the following diagram, at least what percentage of blockage would you expect if the patient experience angina at the goal of exercise?
- 50%
- 70%
- 80%
- 85%
- 90%
You are running a stress test. The patient has resting blood pressure 130/80 and heart rate of 75. The exercise goal is blood pressure 160/120 and heart rate of 150. Using the following diagram, at least what percentage of blockage would you expect if the patient experience angina at the goal of exercise?
- 50%
- 70%
- 80%
- 85%
- 90%
Explanation: Using the double product, we can determine the goal exercise would result in 2.46X in coronary flow (160*150/130/75). If the patient is symptomatic at the exercise goal, the maximal dilation would be below 2.46X. Therefore, the patient would have a 80% blockage based on the figure.
Learning objective:
133a Describe functional testing of stenosis severity
A 48-year-old executive presents to the emergency department because of chest tightness and shortness of breath. ECG shows ST-segment elevations in leads V4, V5, and V6. He has a history of high blood pressure and his father died of heart problems at a young age. Assuming no other cardiac history, which of the following myocardial abnormalities would most likely be seen via light microscopy eight hours after his symptoms began?
A. Contraction bands
B. Granulation tissue
C. Monocytic infiltrate
D. Lymphocytic infiltrate
E. No change can be detected with light microscopy at this time
A 48-year-old executive presents to the emergency department because of chest tightness and shortness of breath. ECG shows ST-segment elevations in leads V4, V5, and V6. He has a history of high blood pressure and his father died of heart problems at a young age. Assuming no other cardiac history, which of the following myocardial abnormalities would most likely be seen via light microscopy eight hours after his symptoms began?
A. Contraction bands
B. Granulation tissue
C. Monocytic infiltrate
D. Lymphocytic infiltrate
E. No change can be detected with light microscopy at this time
Explanation: This man has suffered an MI. He demonstrates two of the five important risk factors for developing heart disease, which include HTN, HL, tobacco use, DM, and a family history of heart disease. The changes that occur in the affected cardiac tissue can be helpful in assessing when the infarct occurred. During the first day after an MI, the affected tissue begins to undergo coagulative necrosis and releases enzymes such as troponin I and CK-MB from the dying cells. Coagulative necrosis is marked in the early stages by preservation of general tissue architecture, with myocytes becoming increasingly eosinophilic. Contraction bands will also be seen, causing myocytes to take on a wavy appearance. Granulation and monocytic infiltrate occurs at about 5-10 days after MI. Lymphocytes are not usually obvious in histological samples after MI.
Learning objective:
130a Explain the pathogenesis of Ischemic Heart Disease (IHD) and relate it to risk factors and treatment.
Elevations in cardiac enzymes are used to diagnose a myocardial infarction. Which cardiac enzyme becomes elevated approximately four hours after an MI and remains elevated 7-10 days afterward?
A. Aspartate aminotransferase
B. Brain natriuretic peptide
C. C-reactive protein
D. Creatine kinase-MB fraction
E. Lactate dehydrogenase
F. Myoglobin
G. Troponin
Elevations in cardiac enzymes are used to diagnose a myocardial infarction. Which cardiac enzyme becomes elevated approximately four hours after an MI and remains elevated 7-10 days afterward?
A. Aspartate aminotransferase
B. Brain natriuretic peptide
C. C-reactive protein
D. Creatine kinase-MB fraction
E. Lactate dehydrogenase
F. Myoglobin
G. Troponin
Explanation:
Cardiac troponin I levels (line A) become elevated in the first four hours after an MI and remain elevated for 7-10 days. It is the most specific protein marker for MI. However CK-MB is the enzyme of choice for detection of re-infarction within the first week. If re-infarction occurs, CKMB levels would again increase, whereas troponin levels remain elevated from the previous event.
A. Third enzyme to be elevated; nonspecific.
B. BNP is elevated in CHF when atria are stretched chronically. Not acutely elevated in MI.
C. CRP is a marker of inflammation. Not used to diagnose MI.
D. CK-MB peak in the first 24 hours and then decrease (line B)
E. LDH (line D) is the last cardiac enzyme to become elevated, on ~day 2 post MI
F. Myoglobin rises and falls within 6 hours post MI. Nonspecific for MI. Not used in the diagnosis of MI.
Learning objective:
130a Define the laboratory tests to confirm the diagnosis of MI.
132a Explain the various diagnostic tools to detect and quantify myocardial injury and necrosi
A 32-year-old African American woman presents to her family physician complaining of fevers, fatigue, weight loss, joint pains, night sweats and a rash on her face that extends over the bridge of her nose. She has also had multiple sores in her mouth over the past few weeks. She had a root canal procedure done about 3 months ago without complications. She has no significant past medical history, but has recently had a urinary tract infection. She denies tobacco, alcohol, and illicit drug use. Laboratory evaluation reveals hemolytic anemia. If she were found to have a cardiac lesion, what would be the most likely pathogenetic cause?
A. Bacteremia secondary to recent dental procedure
B. Aberrant flow causing platelet-fibrin thrombus formation secondary to hypercoagulability and malignancy.
C. Bacteremia secondary to a urinary tract infection
D. Immune complex deposition and subsequent inflammation
E. Left atrial mass causing a ball valve-type outflow obstruction
A 32-year-old African American woman presents to her family physician complaining of fevers, fatigue, weight loss, joint pains, night sweats and a rash on her face that extends over the bridge of her nose. She has also had multiple sores in her mouth over the past few weeks. She had a root canal procedure done about 3 months ago without complications. She has no significant past medical history, but has recently had a urinary tract infection. She denies tobacco, alcohol, and illicit drug use. Laboratory evaluation reveals hemolytic anemia. If she were found to have a cardiac lesion, what would be the most likely pathogenetic cause?
A. Bacteremia secondary to recent dental procedure
B. Aberrant flow causing platelet-fibrin thrombus formation secondary to hypercoagulability and malignancy.
C. Bacteremia secondary to a urinary tract infection
D. Immune complex deposition and subsequent inflammation
E. Left atrial mass causing a ball valve-type outflow obstruction
Explanation: This patient’s signs and symptoms point to a diagnosis of systemic lupus erythematosus (SLE). Libman-Sacks endocarditis is a sterile/inflammatory endocarditis that is commonly associated finding with SLE.
Libman-Sacks endocarditis (LSE) is a type of endocarditis that is not caused by bacteria. It is one of the most common cardiac findings associated with lupus, occurring in up to 25% of SLE patients. The mitral valve is most commonly affected, with small vegetations appearing on both sides of the valve. These vegetations can cause mitral valve leaflet thickening; however, this is usually an asymptomatic process.
A. Infective endocarditis from dental procedure in this patient would be subacute and less likely because of the lack of cardiac structural abnormality.
B. Non-bacterial thrombotic endocarditis is usually associated with GI cancer, but the patient’s history does not suggest to have this diagnosis.
C. Given the symptoms, it is not likely to be an acute endocarditis. Similar to option A, subacute endocarditis is less likely given the lack of structural abnormality.
E. Atrial myxomas are benign cardiac tumors that would not be expected to be seen in a patient with lupus.
Learning objectives:
152a Describe the factors predisposing to and the complications of infective endocarditis
152a Describe the key pathological features of both acute and chronic rheumatic heart disease
What murmur is associated with the pressure abnormality below?
A. Harsh holosystolic murmur at left sternal border without radiation
B. ‘opening snap’ followed by decrescendo low-pitched rumble (diastole) near apex
C. Pansystolic murmur with radiation to the axilla
D. Crescendo-decrescendo murmur at 2ndinterspace (systole) radiating to carotids
E. Decresendo mumur immediately after S2 at 2nd-4thinterspace with radiation to apex
What murmur is associated with the pressure abnormality below?
A. Harsh holosystolic murmur at left sternal border without radiation
B. ‘opening snap’ followed by decrescendo low-pitched rumble (diastole) near apex
C. Pansystolic murmur with radiation to the axilla
D. Crescendo-decrescendo murmur at 2ndinterspace (systole) radiating to carotids
E. Decresendo mumur immediately after S2 at 2nd-4thinterspace with radiation to apex
Explanation: Mitral valve regurgitation. Higher than normal atrial filling during a normally low pressure part of the atrial curve, something must be contributing blood to the atria other than passive filling. Underlying etiologies for other murmurs:
A. Ventricular septal defect.
B. Mitral stenosis
D. Aortic stenosis.
E. Aortic regurgitation.
Learning objectives:
145a Explain normal hemodynamics and the abnormal hemodynamics that are created by mitral stenosis and aortic stenosis, which translate into the physical findings and abnormalities in chest X-ray and echocardiography.
146a Explain the abnormal hemodynamics created by regurgitation of the aortic and mitral valves, which translate into the physical findings and abnormalities in chest X-ray and echocardiography.
A 4-month-old is noted to have a grade 3/6, harsh, systolic ejection murmur heard at the left upper sternal border. The mother reports that the child’s lips occasionally turn blue during feeding. A cardiologist recommends surgery. Later, the physician remarks that the infant’s congenital abnormality was related to a failure of neural crest cell migration. Prior to surgery, which of the following was a likely finding?
A. Atrial septal defect
B. Transposition of great vessels
C. Tricuspid atresia
D. Coarctation of aorta
E. Pulmonary stenosis
A 4-month-old is noted to have a grade 3/6, harsh, systolic ejection murmur heard at the left upper sternal border. The mother reports that the child’s lips occasionally turn blue during feeding. A cardiologist recommends surgery. Later, the physician remarks that the infant’s congenital abnormality was related to a failure of neural crest cell migration. Prior to surgery, which of the following was a likely finding?
A. Atrial septal defect
B. Transposition of great vessels
C. Tricuspid atresia
D. Coarctation of aorta
E. Pulmonary stenosis
Explanation: The presentation of cyanotic spells with activity (feeding) are most consistent with Tetralogy of Fallot (TOF), a congenital cardiac defect characterized by (1) pulmonic stenosis, (2) ventricular septal defect, (3) overriding aorta, and (4) right ventricular hypertrophy. The murmur is consistent with pulmonary stenosis.
A. Atrial septal defect (ASD), a non-cyanotic heart lesion, is not a component of TOF. ASDs often do not present until reversal of the left to right shunt due to development of secondary pulmonary hypertension (Eisenmenger syndrome).
B. Transposition of the great vessels (aorta and the pulmonary artery) is another cyanotic congenital cardiac abnormality that will present at birth or shortly thereafter. However, it is not associated with abnormal heart sounds.
C. Tricuspid atresia is a cardiac defect in which the tricuspid valve is missing or abnormally developed, blocking blood flow from the right atrium to the right ventricle. A cyanotic lesion, it will present with bluish skin from birth.
D. Coarctation of the aorta is a narrowing of the aorta that results in decreased blood pressure in the legs compared to the arms. It can present with leg pain on exercise.
Learning objective:
151a
Describe the pathology and pathophysiology of major forms of congenital heart diseases.
Explain the pathogenesis of Eisenmenger’s syndrome
A 4-year-old Caucasian male suffers from cyanosis and dyspnea relieved by squatting. What is the mechanism for the symptomatic relief?
A. Increased right heart pressure leading to better flow in the pulmonary circulation and better oxygenation.
B. Increased systemic resistance resulting in higher left ventricular pressure.
C. Increased left side pressure leading to reverse flow in the atrial septal defect.
D. Increased flow from pulmonary circulation to systemic circulation.
A 4-year-old Caucasian male suffers from cyanosis and dyspnea relieved by squatting. What is the mechanism for the symptomatic relief?
A. Increased right heart pressure leading to better flow in the pulmonary circulation and better oxygenation.
B. Increased systemic resistance resulting in higher left ventricular pressure.
C. Increased left side pressure leading to reverse flow in the atrial septal defect.
D. Increased flow from pulmonary circulation to systemic circulation.
Explanation: The patient has what’s called a “tet-spell,” and should prompt thinking about tetralogy of Fallot: 1) infundibular pulmonary stenosis; 2) ventricular septal defect; 3) right ventricular hypertrophy; and 4) overriding aorta. The cyanotic symptom is due to increased right to left shunt as a result of pulmonary stenosis, VSD and overriding aorta. Squatting increase systemic vascular resistance, thereby increasing left ventricular pressure and reduce the right to left shunting.
Learning objective:
150a Define a congenital complex and contrast this with an individual anomal
150a Describe Tetralogy of Fallot and contrast cyanotic Tetralogy of Fallot from acyanotic Tetralogy of Fallot
Baby A was a 3,180 g male infant born by spontaneous vertex delivery at 38 weeks gestational age. The mother, a 29-year-old gravida 2, para 1, had an uneventful antenatal period with normal prenatal ultrasound scans. She had normal serology and no history of sepsis. The labor and delivery were uncomplicated, and Baby A was born in good condition. At his first newborn physical examination at 12 hours of age, Baby A appeared morphologically normal, with a normal cardiac examination. He bottle-fed well over day 1 and was discharged home with his mother on day 2.
Both mother and infant were reviewed daily by the community midwifery team. However, on day 4, the infant was noted by his mother to be increasingly tachypneic, and his feeding had deteriorated. The infant was evaluated by the general practitioner, who referred him to the regional NICU for ongoing care.
On clinical examination in the NICU, the infant was found to be irritable but alert. There was mild cyanosis in room air. He was tachypneic with a respiratory rate of 80 to 90 breaths per minute, a labored respiratory pattern, and mild subcostal retractions. Breath sounds were clear on auscultation.
The heart rate was regular, and on auscultation, there was a grade 3/6 systolic murmur
loudest over the left lower sternal margin, a gallop rhythm, and right ventricular heave. The femoral pulses were difficult to palpate, but brachial pulses were present. The liver edge was palpable 1cm below the right coastal margin.
What is the first step of management?
A. Start prostaglandin E infusion.
B. Obtain CT of the chest.
C. Prepare for emergency open-heart surgery.
D. Prepare for emergency balloon septostomy.
Baby A was a 3,180 g male infant born by spontaneous vertex delivery at 38 weeks gestational age. The mother, a 29-year-old gravida 2, para 1, had an uneventful antenatal period with normal prenatal ultrasound scans. She had normal serology and no history of sepsis. The labor and delivery were uncomplicated, and Baby A was born in good condition. At his first newborn physical examination at 12 hours of age, Baby A appeared morphologically normal, with a normal cardiac examination. He bottle-fed well over day 1 and was discharged home with his mother on day 2.
Both mother and infant were reviewed daily by the community midwifery team. However, on day 4, the infant was noted by his mother to be increasingly tachypneic, and his feeding had deteriorated. The infant was evaluated by the general practitioner, who referred him to the regional NICU for ongoing care.
On clinical examination in the NICU, the infant was found to be irritable but alert. There was mild cyanosis in room air. He was tachypneic with a respiratory rate of 80 to 90 breaths per minute, a labored respiratory pattern, and mild subcostal retractions. Breath sounds were clear on auscultation.
The heart rate was regular, and on auscultation, there was a grade 3/6 systolic murmur
loudest over the left lower sternal margin, a gallop rhythm, and right ventricular heave. The femoral pulses were difficult to palpate, but brachial pulses were present. The liver edge was palpable 1cm below the right coastal margin.
What is the first step of management?
A. Start prostaglandin E infusion.
B. Obtain CT of the chest.
C. Prepare for emergency open-heart surgery.
D. Prepare for emergency balloon septostomy.
Explanation: The baby is likely having coarctation of aorta above the ductus level. The patent ductus during the first few days allow for normal flow, but the gradual closure of the ductus removes a shunt from pulmonary circulation to systemic circulation, and inadequate oxygenation below the coarctation can result in cyanosis. The most important thing at this stage is to maintain the shunt by infusing prostaglandin E. Balloon septostomy is used only in transposition of great arteries in which the existing shunting is not sufficient to maintain the mixing of oxygenated and deoxygenated blood and there is a need to create second communication between the two blood pools.
Learning objective:
150a Define a congenital complex and contrast this with an individual anomaly
150a Describe the natural history of shunts and the typical pathophysiological changes that can ensue from shunts at various levels
150a Define obstruction, and describe the various obstructions that can be found at different anatomic levels on both the right and left sides of the heart
Which of the following anomaly likely results in right heart hypertrophy?
A. Patent ductus arteriosus.
B. Ventricular septal defect at the outflow track.
C. Atrial septal defect.
Which of the following anomaly likely results in right heart hypertrophy?
A. Patent ductus arteriosus.
B. Ventricular septal defect at the outflow track.
C. Atrial septal defect.
Explanation: The only scenario that would result in increase flow of blood into the right ventricle is ASD. Other two pathologies would result in increase flow of blood through the left side of the heart.
Learning objective:
150a Describe the natural history of the various obstructions, and the typical pathophysiological changes that can ensue
