Week 2 Flashcards
Contrast the pathogenesis of two potential causes of aortic stenosis
The patient may have a congenitally bicuspid aortic valve, in which progressive calcification occurs in the midline raphe and within the cusps. The calcified masses protrude into the sinuses of Valsalva and prevent complete opening of the valve (stenosis).
Alternately, the patient may have an acquired bicuspid valve secondary to rheumatic heart disease (RHD). In RHD, post-inflammatory scarring produces commissural fusion and a conjoined cusp, leading to stenosis.
Explain why a crescendo-decrescendo systolic ejection murmur is heard ina patient with aortic stenosis
The crescendo-decrescendo systolic ejection murmur is auscultated because of the blood flows across the patient’s stenotic aortic valve. As the pressure in the left ventricle increases during systole, blood flow across the rigid aortic valve increases and intensifies the murmur (crescendo). As the pressure in the ventricle decreases, forward blood flow decreases and the murmur lessens in intensity (decrescendo).
Correlate the patient’s angina to the pathophysiology of aortic stenosis.
Angina occurs because there is substantial imbalance between myocardial oxygen supply and demand. This imbalance is due to the concentric hypertrophy of the LV that occurs as a compensatory response to the sustained increase in afterload due to stenosis of the aortic valve. The thickened LV wall requires a greater than normal perfusion. Over time, the compliance of the LV is reduced causing an increase in the wall stress and elevating the LV diastolic pressure (known as diastolic dysfunction). This results in a reduction in the coronary perfusion pressure gradient between the aorta and myocardium. The overall result is an increase in the oxygen demand with a subsequent decrease in the oxygen supply, which causes angina.
Discuss how the patient’s aortic stenosis affects the end diastolic pressure-volume relationship.
The increase in afterload as a result of the aortic stenosis induces concentric hypertrophy of the left ventricle (increase in left ventricular wall thickness). These changes in the ventricular structure would result in a reduction in compliance (i.e. stiffer ventricle), thereby reducing the end diastolic volume (decreased filling) and increasing the end diastolic pressure. This would increase the slope of (shift upward) the end diastolic pressure-volume relationship
Describe the murmur most likely auscultated with mitral valve prolapse
The patient’s mitral valve regurgitation would result in an apical pansystolic (holosystolic) murmur that radiates toward the left axilla.
Because of the incompetent mitral valve, there is immediate retrograde flow across the regurgitant (“leaky”) valve. The murmur begins as soon as ventricular systolic pressure exceeds atrial pressure, when S1 occurs. The uniform intensity of the murmur reflects the continued pressure gradient between the left ventricle and left atria throughout systole. If the left ventricular pressure remains greater than that in the left atrium at the time of aortic closure, then the murmur will continue beyond S2.
Discuss why this patient does not experience dyspnea in the presence of mitral valve regurgitation.
The patient has a known history of mitral valve regurgitation making it a chronic (long-standing) condition, which allows for compensation over time. A portion of the left ventricular stroke volume is regurgitated back into the left atrium (LA) during systole; to compensate, the LA undergoes eccentric hypertrophy resulting in dilation of the LA with an increase in compliance. This allows the chamber to accommodate the larger volume without significant increases in pressure. This chronic adaptive change prevents significant increases in pulmonary vascular pressures. Since the regurgitant effects on the pulmonary circulation are minimal, the patient does not experience dyspnea.
Contrast the primary morphologic changes in this patient’s mitral valve with the secondary changes that will likely develop due to prolapse-induced stress and injury.
The primary gross morphologic change seen in mitral valve prolapse (MVP) is ballooning of enlarged, thickened, and rubbery mitral leaflets. Associated chordae tendinae may be thin and elongated, and the annulus dilated. Histologically, the spongiosa layer of the valve is thickened due to deposition of myxomatous material (myxomatous degeneration), and the collagenous fibrous layer is attenuated.
Secondary changes to the mitral valve include fibrous thickening at points of friction and thrombi formation. Friction-induced injury may also cause fibrosis of the left atrial and/or ventricular mural endocardium. Focal calcifications may develop at the base of the posterior valve leaflet.
Calculate the patient’s ejection fraction ( estimated end diastolic volume (EDV) is 240 mL, and the end systolic volume (ESV) is 185 mL) and relate the left ventricular structural changes (reveals wall thinning and an increase in the left ventricular radius) to its function.
The patient’s calculated ejection fraction is ~23% (240-185 / 240*100).
The TTE findings are consistent with left ventricular dilation. The enlargement could be due to a number of factors that induce a sustained volume overload. To compensate there is a synthesis of new sarcomeres in series with the old causing elongation of the myocytes. This results in eccentric hypertrophy with enlargement of the chamber radius in proportion to the thickness of the wall to try and reduce the wall stress. However, excessive hemodynamic burden can cause the chamber to dilate out of proportion to the wall thickness leading to systolic dysfunction. This impairs contractility, diminishing capacity to eject blood. This reduction in function is noted by the patient’s reduced ejection fraction.
Justify why the etiology of the patient’s symptoms (with increasing dyspnea, dependent edema, fatigue, and orthopnea) over the past month is a result of a reduced ventricular contractility.
The patient’s dilated left ventricle is associated with a higher end systolic volume and reduced stroke volume. In addition, her ejection fraction is reduced. This would indicate that her symptoms over the last month are due to a reduction in her ventricular contractility (shift in the ESPVR downward) leading to a reduced cardiac output preventing balance of the body’s metabolic demand causing the patient’s fatigue. In addition, the loss of ventricular contractility leads to increased hydrostatic pressures in the pulmonary circulation, causing pulmonary edema/congestion resulting in rales, dyspnea, and paroxysmal nocturnal dyspnea.
Predict the cardiac screening OSE findings in left sided heart failure
the main areas of tissue texture change/somatic dysfunction are bilateral parasympathetic viscerosomatic reflexes at the Occiput, C1, and C2, sympathetic viscerosomatic reflexes at the T1-T5 paraspinal musculature, Chapman’s reflexes located at the T2 transverse processes and 2nd intercostal spaces, and possible myofascial trigger points at the 5th intercostal space midway between the sternum and midclavicular line (nipple line).
Since this pathologic cardiac process has been ongoing for a prolonged period as evidenced by the patient’s history and increase in the left ventricular radius, the tissue texture changes at these areas would feel cool, dry, ropy, and fibrotic with a rapidly fading and blanching erythema friction rub (red reflex), indicating a chronic dysfunction. The restrictive barriers for any identified segmental somatic dysfunctions would have a rubbery (not firm) end feel.
Identify two supplements/herbs that may benefit a patient with left sided heart failure
Coenzyme Q10 is found in the highest concentrations in myocardial mitochondria, where it facilitates energy (ATP) production (via the electron transport chain). CoQ10 has beneficial effects on ejection fraction, end-diastolic volume index, and CHF symptoms; however, withdrawal of CoQ10 supplementation may trigger worsened cardiac function and symptoms.
L-Carnitine acts as the “shuttle” for fatty acids into the mitochondria (for ATP production) and is concentrated within the left ventricle. Propionyl-L-Carnitine has been shown to improve ventricular function, reduce systemic vascular resistance (lower blood pressure), increase exercise tolerance, and reduce mortality due to dilated cardiomyopathy
Relate the pathophysiology of critical coarctation of the aorta to justify the use of prostaglandin in this infant.
critical coarctation of the aorta (CoA), which affects the descending aorta and is typically located at the insertion of the ductus arteriosus just distal to the left subclavian artery. CoA is an obstructive congenital heart defect with ductal-dependent systemic blood flow. The acyanotic presentation and timing of this patient’s decompensation correlating with physiologic closure of the ductus arteriosus supports the diagnosis. The physical examination findings indicate a difference in pre-ductal (upper extremities) and post-ductal (lower extremities) pulses, blood pressure, and oxygen saturation.
In order to re-establish flow to the lower extremities, prostaglandin is given to relax (re-open) the smooth muscle of the ductus arteriosus, which re-establishes systemic blood flow past the level of coarctation through the pulmonary artery to the descending aorta temporarily until definitive surgical repair.
Sxs of coarctation of the aorta
for acute onset of sleepiness and decreased feeding. He was born at term by spontaneous vaginal delivery to a mother with an uncomplicated pregnancy. Physical exam is significant for a lethargic, acyanotic infant. His brachial pulses are strong, but his bilateral femoral pulses cannot be palpated. Blood pressure and oxygen saturation are higher in his upper extremities compared to his lower extremities. A systolic ejection murmur is heard at the apex of the heart.
Describe the cardiopulmonary changes occurring at and soon after birth that facilitate the transition from fetal to neonatal circulation.
In order to facilitate the transition from fetal to neonatal circulation, three general changes occur, including decreased pulmonary pressure, increased systemic pressure, and closure of the fetal shunts.
Decreased pulmonary pressure occurs because alveolar fluid is cleared from the lungs during the birthing process, lungs are expanded with air with the infant’s first breath, and the pulmonary vascular resistance decreases due to rising oxygen content in the lungs.
Increased systemic pressure occurs when the umbilical cord is clamped and the low-resistance placenta is removed. Clamping of the umbilical cord also stops flow from the umbilical vein and removes the volume load to the right side of the heart.
With the overall decrease in pulmonary pressure and increase in systemic pressure, blood flow reverses through the fetal shunts, which directly closes the foramen ovale and contributes to closure of the ductus arteriosus. After reversal of blood flow due to the change in pressure gradient at birth and onset of gas exchange in the lungs, the ductus arteriosus receives highly oxygenated blood from the aorta to the pulmonary artery. Oxygen constricts and functionally closes the ductus arteriosus around 24 to 48 hours (up to 96 hours of life) in a term infant.
Describe V-tach and rerelate it to the underlying etiology of his electrocardiographic changes.
The patient’s cardiac rhythm represents ventricular tachycardia, which is characterized by monomorphic widened QRS complexes at a heart rate of ~162 bpm (27 QRS complexes in 10 seconds).
The underlying etiology of this rhythm is acute myocardial ischemia/ infarction (with symptoms typical of acute coronary syndrome in the setting of established heart disease). Ischemia changes the resting membrane potential and the inward and outward ionic fluxes during the action potential. This leads to alterations in impulse formation and conduction (including the formation of reentrant circuits), refractoriness, and abnormal automaticity of cardiac muscle cells, all of which contribute to the occurrence of ventricular arrhythmias.
