Cardiology Core Curriculum A problem-based approach - part 6 pot

at the flat portion of the Starling curve. This may require a reduction in the diuretic dose or even a “diuretic holiday” for 1 or 2 days in order to introduce ACE inhibitors. A slow upward titration will also increase the likelihood that targeted doses will be reached. Adverse reactions include the development of an ACE inhibitor- induced cough; this is mediated by bradykinins, which are increased with ACE inhibition. No specific therapy is effective in relieving cough. Patients either cope with antitussives or discontinue therapy. Less frequently, development of angioneurotic edema, drug eruptions, and rarely drug-induced neutropenia occur. ACE inhibitors are contraindicated in pregnancy. Several points regarding ACE inhibitor therapy for heart failure should be remembered. • ACE inhibitors are indicated in all patients with heart failure and left ventricular systolic dysfunction. • Therapy should mimic that of the major survival trials in terms of dose and agent selected. • ACE inhibitors should not be suspended or discontinued because of hypotension unless the patient is symptomatic. This is because of the interrelationship between blood pressure (BP), cardiac output (CO) and systemic vascular resistance (SVR), which is defined by BP = CO × SVR. Even though ACE inhibitors and other vasodilators decrease SVR, the corresponding increase in CO offsets any drop in BP unless the patient is volume depleted. Angiotensin II receptor antagonists These agents competitively inhibit the receptors for angiotensin II, and there is a lack of associated cough because there is no effect on bradykinins. The weight of evidence suggests that these agents should be considered in patients being treated with digitalis, diuretics, and a β-blocker who cannot tolerate an ACE inhibitor because of cough or angioedema. 5 ββ -Blockers Activation of the sympathetic nervous system adversely influences the course of chronic heart failure. Until relatively recently, it was thought that β-adrenoreceptor antagonists were contraindicated in heart failure because of their negative inotropic effects. However, it has emerged that several β-blockers (carvedilol, 12 bisoprolol, and extended release metoprolol) improve mortality and quality of life, and reduce Cardiology Core Curriculum 308 hospitalization in patients with mild to moderate (New York Heart Association class II or III) heart failure. 13 Initiation of this therapy requires individualized drug dosing and very careful clinical monitoring. Additional therapy for congestive heart failure Electrolyte supplementation is frequently required in patients on significant diuretic doses. Potassium supplementation is most frequently required but can cause gastrointestinal irritation. The usual supplemental dose required is 20–120 mEq/day (20–120 mmol/day). If higher doses are required, then concomitant use of a potassium- sparing diuretic should be considered. Hypokalemia may be difficult to correct without first correcting hypomagnesemia, because Mg 2+ is a cofactor for the Na + /K + -ATPase pump. Magnesium supplementation is difficult because serum measures do not accurately reflect magnesium stores. The oral supplements are poorly absorbed, which also makes repletion difficult. If renal function is normal, then the dose of magnesium is 14 mEq (14 mmol) three to four times daily. Anticoagulants are often given to patients with marked impairment in systolic function, or dilated cardiomyopathy to protect against the development of formation of mural thrombus and possible systemic embolization, which may result in strokes or pulmonary emboli. 14 Certainly, anticoagulants should be given to patients at highest risk (i.e. those with multiple risk factors for emboli [atrial fibrillation, mitral valve disease] or prior embolic events). Warfarin sodium is the preferred agent and should be given to adjust the International Normalized Ratio to 2·0. Amiodarone is a class III antiarrhythmic that has shown some promise in small trials of heart failure patients. It causes a slower heart rate and mild vasodilatation, and suppresses arrhythmias, but it does not reduce the incidence of sudden death or prolong survival. 15 Many patients with heart failure require care in a critical care setting where parenteral agents are used. The available agents include the following: • intravenous nitroglycerin, which causes preload reduction • intravenous nitroprusside, which reduces afterload • dobutamine, which stimulates cardiac contractility and increases cardiac output • dopamine, which at low doses improves renal blood flow; at moderate doses it stimulates cardiac contractility, and at higher doses it causes systemic vasoconstriction and raises blood pressure • milrinone, which causes vasodilatation and augmented cardiac output by inhibiting phosphodiesterase. Heart failure and cardiac transplantation 309 Cardiac transplantation Advances in candidate selection, surgical techniques, postoperative care, immunosuppression, surveillance for rejection, and avoidance of severe infection has resulted in dramatic improvements in survival since the introduction of cardiac transplantation in 1968. One year survival rates now average 80%, and in selected centers the 1 year survival exceeds 90%. Five year survival is approximately 70%. The major limitation to cardiac transplantation is the availability of donor organs, and not every patient who can benefit from cardiac transplantation will receive a heart. The task for transplant committees is to decide who are the best candidates for this limited resource (Box 10.2). Box 10.2 Heart transplantation When to refer for transplantation? Left ventricular ejection fraction <<0·20 Class IV congestive heart failure Intractable arrhythmias that are not amenable to other therapy Refractory ischemia despite efforts at revascularization Poor exercise capacity by objective criteria Marked hyponatremia Fluctuating renal/hepatic function Contraindications Severe comorbidities Intrinsic renal, hepatic, or pulmonary disease Severe peripheral vascular disease Insulin-dependent diabetes with end-organ complications Recent stroke Recent pulmonary infarction Active infection or malignancy Psychosocial instability Case studies Case 10.1 A 43-year-old male executive with positive risk factors for coronary artery disease including obesity, hypertension, smoking, and hyperlipidemia presented acutely with substernal chest pain. The character of the pain was consistent with angina pectoris. The patient is an active, 20 pack-year smoker, with hypertension treated for 5 years with calcium channel blockers and hyperlipidemia. Blood pressure was 160/90 mmHg 3 months previously. Cardiology Core Curriculum 310 Examination. Physical examination: the patient appeared morbidly obese (305 lb [138·6 kg]). Height: 68 inches (172·7 cm). No abnormalities of skin, nail beds, or oral mucosa. Pulse: 92 beats/min, normal character. Blood pressure: 110/70 mmHg in right arm. Jugular venous pulse: normal. Cardiac impulse: normal. First heart sound: normal. Second heart sound: split normally on inspiration. Fourth heart sound present. No murmurs. Two component friction rub heard. Chest examination: normal air entry, no rales or rhonchi. Abdominal examination: soft abdomen, no tenderness, and no masses. Normal liver span. No peripheral edema. Femoral, popliteal, posterior tibial, and dorsalis pedis pulses: all normal volume and equal. Carotid pulses: normal, no bruits. Investigations. Chest x ray: cardiomegaly with clear lung fields. Electrocardiogram: 2 mm flat ST depression in leads I, aVL, V 5 , V 6 ; T-wave inversions in leads V 4 –V 6 . Electrolytes: potassium 3·6 mEq/l (3·6 mmol/l); creatinine 1·9 mg/dl (168 µmol/l); glucose 165 mg/dl (9·1 mmol/l). Serial cardiac enzymes: creatinine kinase-MB 79–96–54 units (normal range 0–3). Echocardiogram: inferolateral hypokinesis; mild mitral regurgitation; left ventricular dimension 5·8 cm (normal <5·5 cm); left ventricular septum 1·6 cm; left ventricular posterior wall 1·5 cm (normal <1·1 cm); small pericardial effusion; left ventricular ejection fraction 0·27. Exercise stress test: the patient exercised for 12 min on a modified Bruce protocol to peak heart rate 140 beats/min, peak systolic blood pressure 190 mmHg, MET level 6·5 (consistent with peak oxygen consumption of 23 ml/kg per min). No anginal symptoms or ST-T changes on electrocardiogram during exercise. Hospital day 5. The patient is ambulating and is asymptomatic, with normal vital signs and cardiac examination, except for presence of a fourth heart sound on auscultation. Questions 1. What diagnosis or diagnoses are applicable? (A) Congestive heart failure. (B) Pericarditis. (C) Q-wave myocardial infarction. (D) Non-Q- wave myocardial infarction. (E) A and C. (F) B and D. (G) A, B, and C. 2. Based on the diagnosis and clinical course, what would be the best medical regimen at the time of discharge? (A) The patient is not ready for discharge; additional procedures need to be done. (B) Aspirin, lipid lowering therapy, and calcium channel blocker (nifedipine). (C) β-blocker (propanolol). (D) Aspirin, ACE inhibitor, β-blocker, and lipid lowering medication. (E) No medical therapy is indicated. 3. Which of the following findings confirm the diagnosis of CHF in this case? (A) Left ventricular ejection fraction below 0·30. Heart failure and cardiac transplantation 311 (B) Dilated left ventricle. (C) History of hypertension. (D) All of these. (E) None of these. 4. Is this patient a candidate for eventual heart transplantation? (A) Yes – he has reduced left ventricular function with an ejection fraction under 0·30 and reduced exercise capacity, with an estimated maximal oxygen consumption below 30 ml/kg per min. (B) No – his clinical course is inconsistent with the indications for transplantation. Answers Answer to question 1 F. This patient has had a non-Q-wave myocardial infarction complicated by pericarditis. The electrocardiographic findings rule out a Q-wave myocardial infarction. The diagnosis of an acute myocardial infarction is confirmed by the diagnostic enzyme pattern. Pericarditis is confirmed by the presence of a pericardial friction rub and a small pericardial effusion. The important concept arising from this question is that the diagnosis of CHF cannot be made on the basis of an abnormal measure of left ventricular function. The left ventricular ejection fraction is reduced and suggests a poor prognosis, but is not sufficient for the diagnosis of CHF. Remember that, for the diagnosis of CHF to be confirmed, there must be both evidence of ventricular dysfunction and evidence of symptoms due to ventricular dysfunction. This patient has asymptomatic left ventricular dysfunction after a myocardial infarction. Answer to question 2 D. Asymptomatic left ventricular dysfunction following myocardial infarction represents a newly appreciated area of left ventricular dysfunction that is clinically important. Patients with left ventricular dysfunction after myocardial dysfunction go on to develop eventual CHF, recurrent myocardial infarction, and premature death. The use of ACE inhibitors in this group of patients has been associated with an improvement in survival, a reduced likelihood of development of heart failure, and a reduced rate of recurrent myocardial infarction. β-Blockers and aspirin are indicated after myocardial infarction. The addition of lipid lowering therapy is specific for this patient, given the history of a significant but untreated hyperlipidemia. There is no indication for most types of calcium channel blockers after myocardial infarction, and their routine use is usually contraindicated, especially in patients with known pulmonary congestion and ventricular dysfunction. This is probably due to their negative inotropic properties. Based on this patient’s benign clinical course, a cardiac catheterization after myocardial infarction is not indicated. Cardiology Core Curriculum 312 Answer to question 3 E. Again, this patient does not have CHF but rather has asymptomatic left ventricular dysfunction. All of the descriptors are valid, including depressed left ventricular function, dilated left ventricle, and prior history of hypertension, but again the lack of symptoms prevents one from making a diagnosis of heart failure. Answer to question 4 B. The data listed in A are not indications for heart transplantation. A maximal oxygen consumption greater than 20 ml/kg per min is consistent with a good short-term prognosis and does not suggest that transplantation is indicated. Similarly, heart transplantation is not done on the basis of a depressed left ventricular ejection fraction alone. Case 10.2 A 21-year-old gardener with no prior history of cardiac disease or positive risk factors presented after 6 weeks of a persistent complaint of a “cold”. He describes the onset of a severe flu-like illness that caused him to miss 4 days of work 6 weeks ago. He recovered partially after bed rest and fluids, but had a persistent cough. He attempted to return to work after 1 week but had cough and fatigue. He saw a nurse practitioner who diagnosed bronchitis and pleurisy based on a productive cough and basilar rhonchi. Two weeks of oral antibiotics did not resolve his symptoms. He once again stopped work and visited an internist. A work up for mononucleosis and Epstein–Barr virus was instituted, and the antibiotics were changed to erythromycin to cover atypical pneumonias. A CD4 count was borderline normal. The patient had one homosexual encounter 2 years ago. After 2 more weeks of malaise, cough, and fatigue, the patient developed difficulty sleeping and vague abdominal discomfort. He then presented to a university hospital emergency room where he was evaluated by a senior medical student. He did not use tobacco or alcohol, and had no prior illnesses. Examination. Physical examination: the patient appeared seriously ill. Extremities cool. Pulse: 120 beats/min, with pulsus alternans. Blood pressure: 80/60 mmHg. Jugular venous pulse: 12 cm at 45°. Parasternal lift. First heart sound: normal. Second heart: normal. Third and fourth heart sounds were present, along with a grade 3/6 mitral holosystolic murmur. Chest examination: diffuse crackles to mid-chest. Abdominal examination: soft abdomen, liver span 16 cm. No peripheral edema. Femoral and popliteal pulses: all palpable and equal. Carotid pulses: normal, no bruits. Investigations. Chest x ray: markedly enlarged cardiac shadow; blunted costophrenic angles; enlarged pulmonary arteries; diffuse Heart failure and cardiac transplantation 313 pan-lobar infiltrates in an alveolar pattern. Electrocardiogram: sinus tachycardia, biatrial overload, prominent voltage, diffuse non-specific ST-T wave changes. Laboratory tests: hemoglobin 12 g/dl (120 g/l), sodium 131 mEq/l (131 mmol/l), creatinine 2·2 mg/dl (194 µmol/l), aspartate aminotransferase 125 U/l (2·1 µkat/l; normal range 0–0·58 µkat/l), alanine aminotransferase 100 U/L (1·7 µkat/l), alkaline phosphatase 235 U/l (Normal range 30–120 U/l); total bilirubin 2·1 mg/dl (36 µmol/l; normal range 5·1–17 µmol/l); thyroid function tests normal. Echocardiogram: severe depression of left ventricular systolic function, left ventricular diastolic diameter 8·2 cm (normal <6 cm), left ventricular ejection fraction 0·15, dilated left atrium, moderately severe mitral insufficiency, moderate tricuspid insufficiency, estimated right ventricular systolic pressure 56 mmHg. Right heart catheterization: cardiac output 2·8 l/min (normal >4·0 l/min), right atrium 20 mmHg (normal 2–10 mmHg), right ventricle 60/20 mmHg (normal range 15–30/2–10 mmHg), pulmonary artery 60/35 mmHg (normal range 15–30/5–10 mmHg), wedge pressure 33 mmHg (normal 5–14 mmHg), mixed venous saturation 49% (normal >60%), systemic vascular resistance 1428 dynes·s/cm 5 (143 kPa·s/l). Endomyocardial biopsy: normal myocardial cells with sparse interstitial inflammatory infiltrate. Hospital day 3. For the first 2 hospital days the patient was treated with oral medications while undergoing the hospital evaluation outlined above. He remained uncomfortable throughout the first 48 hours. The patient awoke with nausea and extreme malaise. His blood pressure was 65 mmHg. He had a witnessed syncopal episode with telemetry demonstrating a wide complex tachycardia at 175 beats/min. Emergent direct current cardioversion was required twice. The patient was transferred to intensive care unit. A right heart catheter was placed, with findings identical to those noted above. Hospital day 20. After intensive medical therapy the patient was recovering well. He became ambulatory. His blood pressure was 116/70 mmHg and his heart rate was 68 beats/min. His cardiac examination was normal. Repeat echocardiography revealed a left ventricular ejection fraction 0·25 with a small apical shadow, consistent with a ventricular clot. Three months later, echocardiography demonstrated an ejection fraction of 0·54. One month later he returned to his usual employment. Questions 1. The diagnosis of CHF was not originally suspected because of which of the following? (A) The patient had no clinical evidence of heart disease at the onset of his illness. (B) The patient’s demographics were atypical for the diagnosis of heart Cardiology Core Curriculum 314 failure. (C) No signs or symptoms of heart failure were present at the onset of his illness. (D) The diagnosis of CHF can be difficult to discriminate from atypical pneumonia. (E) A and C. (F) B and D. 2. At the time of hospital presentation, this patient had CHF of what severity? (A) Class I. (B) Class II. (C) Class III. (D) Class IV. (E) The patient did not have CHF at the time of presentation. 3. The diagnostic right heart catheterization revealed which hemodynamic profile? (A) Increased preload. (B) Decreased afterload. (C) Increased afterload. (D) Normal cardiac index. (E) A and C. (F) B and D. (G) None of the above. 4. The hemodynamic findings are consistent with which of the following? (A) Septic shock. (B) Cardiogenic shock. (C) Hypovolemic shock. 5. Regarding the dramatic decompensation on day 3, which of the following statements is correct? (A) Ventricular tachycardia is an unexpected complication. (B) The presence of ventricular tachycardia represents a serious negative prognostic factor. (C) This patient should be treated with antiarrhythmic agents indefinitely in view of this life-threatening episode of ventricular tachycardia. 6. What is the best therapy at the time of transfer to the intensive care unit? (A) Oxygen, high dose oral diuretics, high dose dopamine, and broad spectrum antibiotics. (B) Dobutamine titrated to a cardiac index greater than 2·5 l/min per m 2 , and parenteral diuretics, oxygen, lidocaine, and intravenous nitroprusside. (C) High dose steroid therapy, intravenous immune globulin, and norepinephrine. Answers Answer to question 1 F. This patient had CHF probably due to acute myocarditis. Because he does not represent the usual patient affected with CHF and because upper respiratory illnesses are so common in his age range, the diagnosis of heart failure was missed. This is a frequent occurrence in daily practice. The evidence for heart failure was present in the beginning, with cough and fatigue as well as the resting tachycardia. In this case, the diagnosis of CHF was not made even though symptoms were present. Answer to question 2 D. By the time this patient was admitted the diagnosis of heart failure was obvious and he was critically ill. The presence of symptoms at rest is consistent with class IV CHF, which carries a 70% 1 year mortality. Answer to question 3 E. Heart failure and cardiac transplantation 315 Answer to question 4 B. A review of the hemodynamic profile demonstrates severe left ventricular dysfunction. The cardiac output is severely depressed. The preload is markedly increased, given the pulmonary capillary wedge pressure of 33 mmHg and the central venous pressure of 20 mmHg. The afterload is also increased, based on a calculated systemic vascular resistance in excess of 1400 dynes·s/cm 5 . The profile of severely reduced cardiac output and increased filling pressures with a markedly elevated peripheral resistance is consistent with the diagnosis of cardiogenic shock. Answer to question 5 B. For patients with heart failure the incidence of ventricular arrhythmias approaches 75% and the presence of complex ventricular rhythm disturbances, including ventricular tachycardia, approaches 50%. Ventricular tachycardia is an expected complication of severe heart failure. Despite the prevalence of ventricular arrhythmias in heart failure, no data as yet suggest that medical therapy can modify the rate of death due to sudden cardiac events. Antiarrhythmic therapy is not necessarily indicated on a chronic basis. Nevertheless, when serious ventricular arrhythmias complicate CHF, the prognosis is noted to be quite poor. Answer to question 6 B. At the time of transfer to the intensive care unit, this patient is seriously ill having just been resuscitated from a cardiac arrest. The right heart catheterization confirms poor ventricular function. The goal of management is to improve the cardiac output, reduce the elevated filling pressures, provide supplemental oxygen, and initiate prophylactic therapy for ventricular arrhythmias. The addition of nitroprusside is of benefit because of its vasodilator properties and ability to reduce afterload. The choices listed in A are not inappropriate except for the use of oral diuretics. In a critically ill patient with evidence of central venous pressure elevation and elevated liver function tests consistent with a congested liver, it is unwise to continue to administer oral agents that will have an unpredictable absorption and therefore an unpredictable response. The biopsy evidence of acute myocarditis suggests that immunosuppressive therapy may be of benefit to resolve this acute inflammatory process. The available data demonstrate that the spontaneous recovery rate from such an illness is as high as 40–50%, which is identical to the recovery rate seen with immunosuppressive therapy but without the toxicity of steroids. Supportive care remains the best option for patients with acute onset CHF, even if myocarditis is biopsy proven. Cardiology Core Curriculum 316 Case 10.3 A 69-year-old woman with a longstanding history of essential hypertension presents to the primary care clinic for routine evaluation. She initially denied any specific complaints at the present time. On further questioning she notes that she has had an unexplained weight gain. She also describes frequent episodes of fatigue, which she attributes to “old age”. She is unable to take her evening walk without resting halfway through. Her family thinks she is well and simply needs to rest more frequently. Past history: a 20 year history of documented hypertension, intermittent compliance with medications, and no history of stroke or renal disease; overweight by 30 lb (13·6 kg) for 30 years; and an active 13 pack-year history of smoking. Current medications: verapamil 80 mg three times daily and hydrochlorothiazide 75 mg/day. Examination. Physical examination: the patient appeared normal. Pulse: 96 beats/min, normal character. Blood pressure: 170/95 mmHg. Jugular venous pulse: normal. Cardiac impulse: displaced laterally, diffuse. First heart sound: normal. Second heart sound: split normally on inspiration. No added sounds or murmurs. Chest examination: normal air entry, fine basilar crackles. Abdominal examination: soft abdomen, liver tender to palpation, no masses. Normal liver span. Trace ankle edema. Carotid pulses: normal, no bruits. Investigations. Chest x ray: clear lung fields, cardiothoracic ratio of 0·65. Electrocardiogram: sinus tachycardia, left atrial overload, left ventricular hypertrophy. Laboratory findings: hemoglobin 10 g/dl (100 g/l), creatinine 2·9 mg/dl (256 µmol/l), potassium 3·5 mEq/l (3·5 mmol/l), glucose 160 mg/dl (8·9 mmol/l). Questions 1. Does this patient have CHF? (A) Yes – she has a known history of hypertension. (B) No – there is no assessment of ventricular function to establish the diagnosis of CHF. (C) No – she has poorly controlled hypertension. (D) Yes – she has probable hypertensive heart disease and symptoms of volume overload. (E) There are insufficient data to make the diagnosis. 2. What is the next most appropriate step in the evaluation? (A) Evaluation for coronary artery disease. (B) Echocardiogram. (C) Both A and B. (D) Neither A nor B – all of the data needed are available already. 3. What is the mortality risk over the next year based on the severity of her illness at the present time? (A) 5%. (B) 10–15%. (C) 30%. (D) 70%. Heart failure and cardiac transplantation 317 [...]... Does this patient have abnormal central venous pressure? JAMA 19 96; 275 :63 0–4 4 Report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines Guidelines for the Evaluation and Management of Heart Failure Circulation 1995;92:2 764 –84 5 Hunt SA, Baker DW, Chin MH, et al ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult: executive... 60 mg every 6 hours, hydrochlorothiazide 50 mg/day, and coumadin 5 mg/day 4 After 2 years she began to fail on the above medical therapy She is placed on oxygen at 4 l/min and a continuous prostacyclin infusion Which is the most appropriate treatment option? (A) Surgical repair of congenital heart disease (B) Heart transplantation evaluation (C) Heart lung transplant evaluation (D) Lung transplantation... nifedipine is a vasodilator, its negative inotropic action once again makes it a suboptimal choice in the management of heart failure Only option D includes an appropriate dose of ACE inhibitor, reduced dose of digoxin, loop diuretic, and modest potassium supplementation Case 10.4 A 37-year-old woman 2 years postpartum presents for evaluation of dyspnea She describes a normal pregnancy and a benign postpartum... 11.5 Coarctation of the aorta (postductal type) The area of obstruction is located distal to the left subclavian artery (LSA), near the ligamentum arteriosum (fine arrow) Ao, aorta; LCC, left common carotid artery; PA, pulmonary artery; RCC, right common carotid artery; RSA, right subclavian artery (Thick arrow shows site of coarctation of the aorta) Coarctation of the aorta should be suspected in a young... postoperative restenosis Cyanotic congenital heart disease Tetralogy of Fallot Tetralogy of Fallot accounts for approximately 10% of all congenital heart disease and is the most common cyanotic defect presenting in 335 Cardiology Core Curriculum Ao PA LA RA LV RV Figure 11 .6 Tetralogy of Fallot with left aortic arch (normal orientation) A large non-restrictive ventricular septal defect with an overriding aorta... significant pulmonary hypertension not due to left heart failure has been ruled out The available data have revealed that patients with pulmonary hypertension, that is fixed, do not do well with heart transplantation even if overt heart disease is the major pathology The heart transplant work up for all potential recipients includes a right heart catheterization for this reason A lung transplantation... phenotypic women with primary amenorrhea, short stature, and multiple congenital abnormalities) Bicuspid aortic valves are seen in approximately half of all patients with coarctation of the aorta Other obstructive lesions of the left heart (mitral stenosis, subaortic stenosis, aortic stenosis) are also associated with coarctation of the aorta As many as 20% of cases of coarctation are undetected in childhood,... following? (A) Work up for mediastinal tumors based on the abnormal x ray film (B) Echocardiogram and right heart catheterization (C) Left heart catheterization (D) Connective tissue disease work up (E) A and C (F) B and D 3 After another near syncopal episode she returned and was admitted A Swan–Ganz catheter was placed and demonstrated the following findings: pulmonary artery pressure 90/45 mmHg, pulmonary... lung transplantation for this illness relieves the afterload on the right ventricle and normal function returns A heart–lung transplant is therefore not indicated 321 Cardiology Core Curriculum The 1 year survival for heart–lung transplantation is approximately 50% A heart transplantation alone does not solve the problem with pulmonary hypertension In fact, patients cannot receive a heart transplant until... normal or only mildly enlarged The ascending aorta may appear 334 Congenital heart disease dilated (suggesting a bicuspid aortic valve) A “three” sign may be seen, caused by a dilated left subclavian artery above the coarctation and poststenotic dilatation of the aorta below the coarctation Rib notching is seen in the posterior aspect of the fourth to eighth ribs in older children and adults as a result . diffuse Heart failure and cardiac transplantation 313 pan-lobar infiltrates in an alveolar pattern. Electrocardiogram: sinus tachycardia, biatrial overload, prominent voltage, diffuse non-specific ST-T. most appropriate treatment option? (A) Surgical repair of congenital heart disease. (B) Heart transplantation evaluation. (C) Heart lung transplant evaluation. (D) Lung transplantation evaluation. Answers Answer. vasodilatation and augmented cardiac output by inhibiting phosphodiesterase. Heart failure and cardiac transplantation 309 Cardiac transplantation Advances in candidate selection, surgical techniques,