Breathing Not Properly
Answer: C
This woman presents with the classic triad of advanced aortic stenosis: shortness of breath, chest pain, and dizziness (or syncope).
Aortic disease is most commonly a sequela of rheumatic heart disease (worldwide) or calcific disease (developed countries). Rheumatic heart disease can cause fusion of commissures while calcific disease (often age related, worse with a congenital bicuspid aortic valve) leads to thickened, stiff, relatively immobile leaflets (B).
Aortic stenosis (AS) is a slowly evolving disease with vague non-specific symptoms predominating initially – presentation will vary by age, comorbidities, and baseline level of activity. All symptoms stem from left ventricular outflow obstruction, which causes left ventricular hypertrophy over time (A).
Other classic symptoms include: dyspnea on exertion, decreased exercise tolerance, dizziness with minimal exertion, and angina.
As heart failure is a common complication of AS, it is important not to ascribe all symptoms to worsening heart failure without having established the quality and function of the aortic valve. This is especially apropos for the emergency physician who may anchor the diagnosis of heart failure (due to pattern recognition) without considering aortic disease. Since the patient with severe AS is preload-dependent, abrupt changes in preload – from treatments for ACS or heart failure such as nitrates or diuretics – may cause a dramatic drop in cardiac output, effecting the cerebral and coronary circulations adversely and acutely.
Patients with AS often have concomitant coronary artery disease (C); it is not uncommon for a patient to undergo coronary artery bypass with concomitant aortic valve replacement.
Various dysrhythmias are associated with the consequences of AS, most notably atrial fibrillation. Transient
bradycardias are common after exertion. Ventricular dysrhythmias are rare as the culprit etiology for symptoms in the stable patient with AS.
Patients with AS commonly have angina (approximately 2/3 of patients with AS), and care must be taken to balance the treatment of possible ACS with the need to sustain the delicate balance of preload-dependent cardiac output. Chest pain in patients with AS may be due to true ACS, increased left ventricular myocardial oxygen demand (causing global ischemia), reduced diastolic coronary perfusion (from tachycardia)
Physical examination findings that are readily appreciated in the emergency department include a harsh systolic ejection murmur, delayed carotid upstroke, and displaced point of maximal impact (PMI). In a review, Etchell et al (1997) found that three findings were the most useful for identifying AS: a slow rate of rise in the carotid pulse, mid to late peak intensity of the murmur, and reduced intensity of the second heart sound. Admittedly, these may be difficult to appreciate in a noisy and busy emergency department.
Other helpful physical findings include:
Pulsus alternans: alternating strong and weak pulse quality – in a restrictive hypertrophic cardiomyopathy, decreased filling (poor end-diastolic volume) causes a slightly diminished ejection fraction (the “weak” pulse). Since the left ventricle was under-evacuated, it is “pre-stretched” with residual volume. The next cycle adds filling
volume, resulting in increased end-diastolic filling (from the residual “pre-filling”) as well as increased contractility (from increased Starling forces from the previously stretched myocardium) resulting in the alternating
“strong” pulse.
Pulsus parvus et tardus (weak and delayed pulse) – the carotid pulse may be the easiest to appreciate the
consequence of the left ventricular outflow obstruction.
Definitive treatment is valve replacement. The PARTNER trial showed that patients deemed inoperable had improved survival with transcatheter aortic valve replacement (a bioprosthetic valve mounted on a wire frame is wedged into the native stenotic arotic valve); outcomes in this cohort were similar to those who underwent surgical aortic valve replacement.
Emergent balloon valvotomy is better established in children, adolescents, and young adults. It may be an option as a bridge therapy for older adults until surgery can be performed.
The critical patient with AS:
AS may result in sudden cardiac death due to malignant bradydysrythmias, sustained ventricular tachydysrythmias, or an exaggerated Bezold-Jarisch reflex: an underfilled left ventricle (from dehydration, hemorrhage, orthostatics, MI, etc) triggers a reflex bradycardia (teleologocally to improve filling and therefore cardiac output).
Decompensated heart failure in AS can be treated with nitroprusside (more for the afterload decreasing effects) and/or an intra-aortic balloon pump – only to bridge for a valve replacement in the appropriate
candidate.
Our patient had an emergent echocardiogram that showed an ejection fraction of 50% and an aortic valve area of 1.2 cm2. Her left heart catheterization showed severe three-vessel coronary artery disease, and she underwent aortic valve replacement in conjunction with three-vessel bypass grafting. She did well after surgery, cardiac rehabilitation, and now enjoys a more functional quality of life.
References
Aksoy O, O’Brien BL, Menon V. Options for managing severe aortic stenosis: A case-based review. Cleveland Clinic Journal of Medicine. 2013; 80(4):243-252.
Bonow RO, Carabello BA, Chatterjee K et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of
Patients With Valvular Heart Disease). Circulation. 2006;114:450–527.
Etchells E, Bell C, Robb K. Does this patient have an abnormal systolic murmur? JAMA; 1997; 277:564.
This woman presents with the classic triad of advanced aortic stenosis: shortness of breath, chest pain, and dizziness (or syncope).
Aortic disease is most commonly a sequela of rheumatic heart disease (worldwide) or calcific disease (developed countries). Rheumatic heart disease can cause fusion of commissures while calcific disease (often age related, worse with a congenital bicuspid aortic valve) leads to thickened, stiff, relatively immobile leaflets (B).
Aortic stenosis (AS) is a slowly evolving disease with vague non-specific symptoms predominating initially – presentation will vary by age, comorbidities, and baseline level of activity. All symptoms stem from left ventricular outflow obstruction, which causes left ventricular hypertrophy over time (A).
Other classic symptoms include: dyspnea on exertion, decreased exercise tolerance, dizziness with minimal exertion, and angina.
As heart failure is a common complication of AS, it is important not to ascribe all symptoms to worsening heart failure without having established the quality and function of the aortic valve. This is especially apropos for the emergency physician who may anchor the diagnosis of heart failure (due to pattern recognition) without considering aortic disease. Since the patient with severe AS is preload-dependent, abrupt changes in preload – from treatments for ACS or heart failure such as nitrates or diuretics – may cause a dramatic drop in cardiac output, effecting the cerebral and coronary circulations adversely and acutely.
Patients with AS often have concomitant coronary artery disease (C); it is not uncommon for a patient to undergo coronary artery bypass with concomitant aortic valve replacement.
Various dysrhythmias are associated with the consequences of AS, most notably atrial fibrillation. Transient
bradycardias are common after exertion. Ventricular dysrhythmias are rare as the culprit etiology for symptoms in the stable patient with AS.
Patients with AS commonly have angina (approximately 2/3 of patients with AS), and care must be taken to balance the treatment of possible ACS with the need to sustain the delicate balance of preload-dependent cardiac output. Chest pain in patients with AS may be due to true ACS, increased left ventricular myocardial oxygen demand (causing global ischemia), reduced diastolic coronary perfusion (from tachycardia)
Physical examination findings that are readily appreciated in the emergency department include a harsh systolic ejection murmur, delayed carotid upstroke, and displaced point of maximal impact (PMI). In a review, Etchell et al (1997) found that three findings were the most useful for identifying AS: a slow rate of rise in the carotid pulse, mid to late peak intensity of the murmur, and reduced intensity of the second heart sound. Admittedly, these may be difficult to appreciate in a noisy and busy emergency department.
Other helpful physical findings include:
Pulsus alternans: alternating strong and weak pulse quality – in a restrictive hypertrophic cardiomyopathy, decreased filling (poor end-diastolic volume) causes a slightly diminished ejection fraction (the “weak” pulse). Since the left ventricle was under-evacuated, it is “pre-stretched” with residual volume. The next cycle adds filling
volume, resulting in increased end-diastolic filling (from the residual “pre-filling”) as well as increased contractility (from increased Starling forces from the previously stretched myocardium) resulting in the alternating
“strong” pulse.
Pulsus parvus et tardus (weak and delayed pulse) – the carotid pulse may be the easiest to appreciate the
consequence of the left ventricular outflow obstruction.
Definitive treatment is valve replacement. The PARTNER trial showed that patients deemed inoperable had improved survival with transcatheter aortic valve replacement (a bioprosthetic valve mounted on a wire frame is wedged into the native stenotic arotic valve); outcomes in this cohort were similar to those who underwent surgical aortic valve replacement.
Emergent balloon valvotomy is better established in children, adolescents, and young adults. It may be an option as a bridge therapy for older adults until surgery can be performed.
The critical patient with AS:
AS may result in sudden cardiac death due to malignant bradydysrythmias, sustained ventricular tachydysrythmias, or an exaggerated Bezold-Jarisch reflex: an underfilled left ventricle (from dehydration, hemorrhage, orthostatics, MI, etc) triggers a reflex bradycardia (teleologocally to improve filling and therefore cardiac output).
Decompensated heart failure in AS can be treated with nitroprusside (more for the afterload decreasing effects) and/or an intra-aortic balloon pump – only to bridge for a valve replacement in the appropriate
candidate.
Our patient had an emergent echocardiogram that showed an ejection fraction of 50% and an aortic valve area of 1.2 cm2. Her left heart catheterization showed severe three-vessel coronary artery disease, and she underwent aortic valve replacement in conjunction with three-vessel bypass grafting. She did well after surgery, cardiac rehabilitation, and now enjoys a more functional quality of life.
References
Aksoy O, O’Brien BL, Menon V. Options for managing severe aortic stenosis: A case-based review. Cleveland Clinic Journal of Medicine. 2013; 80(4):243-252.
Bonow RO, Carabello BA, Chatterjee K et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of
Patients With Valvular Heart Disease). Circulation. 2006;114:450–527.
Etchells E, Bell C, Robb K. Does this patient have an abnormal systolic murmur? JAMA; 1997; 277:564.