[vc_row row_type=”row” use_row_as_full_screen_section=”no” type=”full_width” oblique_section=”no” text_align=”left” css_animation=””][vc_column][ultimate_heading main_heading=”Candidate brief” main_heading_color=”#000000″ sub_heading_color=”#000000″ main_heading_style=”font-weight:bold;” main_heading_font_size=”desktop:36px;”]”This patient has presented to the acute medical take following a fall with loss of consciousness. Please examine their cardiovascular system and present your findings to the examiners.”[/ultimate_heading][vc_empty_space image_repeat=”no-repeat”][vc_video link=”https://vimeo.com/138191718″][vc_empty_space image_repeat=”no-repeat”][vc_row_inner row_type=”row” type=”full_width” use_row_as_full_screen_section_slide=”no” text_align=”left” css_animation=””][vc_column_inner width=”1/4″][stat_counter icon_size=”32″ counter_title=”Station Time” counter_value=”20″ counter_suffix=” minutes” speed=”3″][/vc_column_inner][vc_column_inner width=”1/4″][stat_counter icon_size=”32″ counter_title=”Time for this encounter” counter_value=”10″ counter_suffix=” minutes” speed=”3″][/vc_column_inner][vc_column_inner width=”1/4″][stat_counter icon_size=”32″ counter_title=”Maximum time to examine your patient” counter_value=”6″ counter_suffix=” minutes” speed=”3″][/vc_column_inner][vc_column_inner width=”1/4″][stat_counter icon_size=”32″ counter_title=”Minimum time for discussion and questions” counter_value=”4″ counter_suffix=” minutes” speed=”3″][/vc_column_inner][/vc_row_inner][vc_empty_space image_repeat=”no-repeat”][/vc_column][/vc_row][vc_row row_type=”row” use_row_as_full_screen_section=”no” type=”full_width” oblique_section=”no” text_align=”left” css_animation=””][vc_column][/vc_column][/vc_row]
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This patient has an ejection systolic murmur in the aortic area consistent with aortic stenosis – one of the commonest abnormalities encountered in the MRCP PACES.
Aortic stenosis is a common condition, with a normal aortic valve area of between 2-4 cm2 and moderate stenosis defined as 1-1.5 cm2 and severe as <1 cm2. To preserve stroke volume, the left ventricle will often compensate by becoming hypertrophied. Thus, patients may have aortic stenosis for a number of years before becoming symptomatic.
Pure aortic stenosis usually manifests after six to eight decades of progressive obstruction. Onset of symptoms is one to two decades earlier for patients with bicuspid aortic valve disease.
Patients with aortic stenosis presents with:
● Exertional dyspnoea – Reduced left ventricular (LV) compliance elevates both LV diastolic pressure and pulmonary capillary pressure. Dyspnoea accompanies fatigue, exercise intolerance and reduced activity.
● Angina pectoris – develops late due to impaired coronary sinus filling; compression of coronary vessels from hypertrophy and an increased myocardial demand from hypertrophied muscle. Coronary artery disease will commonly be present.
● Syncope. For a static cardiac output, vasodilation in exercising muscle and impaired vasoconstriction in non-exercising muscle causes arterial pressure to drop.
Late-stage aortic stenosis is associated with all the clinical manifestations of impaired cardiac output: weakness, fatigue, peripheral cyanosis and cachexia. In the advanced stage, failure of the left ventricle may co-occur resulting in pulmonary oedema, orthopnoea, and paroxysmal nocturnal dyspnoea in decompensated heart failure.
Findings associated with late, isolated, and severe aortic stenosis:
● Tricuspid regurgitation
● Marked pulmonary hypertension, resulting in:
Right ventricular failure
Systemic venous hypertension
The evaluation of aortic stenosis is typically performed with echocardiography, although cardiovascular magnetic resonance is becoming increasingly common for initial assessment. The echocardiogram is used in the parasternal view to visually assess valvular morphology.
The pressure gradient across the valve (and valve area) is used to estimate the extent of aortic stenosis.
In patients with aortic stenosis, systemic arterial pressure is usually unremarkable. When stroke volume begins to decline, systolic pressure may fall and pulse pressure narrow. A shudder may be palpable, most commonly over the left carotid artery. The a wave in the JVP may become more prominent.
● Auscultation. The murmur of aortic stenosis is classically a mid-systolic ejection murmur heard immediately after S1. It’s heard most reliably over the right second intercostal space. Intensity of the murmur increases until the middle of ejection, drops off, and ends just before closure of the aortic valve. It is heard loudest at the base of the heart, and sounds low-pitched, rasping and rough.
● Echocardiogram. LV hypertrophy, diminished systolic opening of the leaflets, and calcification are usually reported.
● ECG. T-wave inversion in I and aVL due to left ventricular strain with ST depression and evidence of left ventricular hypertrophy.
● Chest Radiography. Cardiac dilation may not manifest until late-stage aortic stenosis. LV hypertrophy with no enlargement rounds the apex. Valve calcification may be apparent in the lateral view, as well as dilation of the ascending aorta in the frontal view. LV enlargement is marked in late-stage aortic stenosis.
● Catheterization. Indicated when other clinical findings are discrepant or in special circumstances due to risk of cerebral embolization.
Aortic stenosis is among the most common forms of valvular heart disease. Gradual calcification can occur in both normal and congenitally abnormal valves. Abnormal cusp development are some of the most common congenital heart defects. Bicuspid aortic valve is are particularly vulnerable to aortic stenosis and aortic insufficiency.
Aortic stenosis appears most commonly in patients with bicuspid aortic valve disease, tri-leaflet deterioration, or prior rheumatic fever. Aortic stenosis is a degenerative calcification of the aortic cusps. Inflammatory signaling, endothelial dysfunction, and lipid accumulation contribute to the disease process.
A pressure gradient is created due to obstructed left ventricular outflow. Because obstruction occurs gradually, concentric LV hypertrophy develops to maintain cardiac performance. When excessive hypertrophy becomes maladaptive, LV systolic function deteriorates and myocardial fibrosis develops. Impaired LV compliance is evident by elevated LV end-diastolic pressure and preserved ejection fraction. In patients with aortic stenosis, cardiac output fails to increase during exercise, but is relatively normal at rest.
Late-stage aortic stenosis has the following pathophysiological features:
● Declining contractile function, cardiac output and the pressure gradient between the LV and aorta
● Increased pulmonary artery, mean left atrial, and RV pressures
● Hypertrophy erodes stroke volume and cardiac output (when ejection fraction is preserved and LV enlargement is absent)
● Left ventricular hypertrophy increases myocardial O2 demands.
● Digoxin, diuretics and sodium restriction before operation are indicated in patients with reduced cardiac reserve
● Enlargement of the aortic root can be addressed with beta blockers, angiotensin receptor blockers and ACE inhibitors
● Valvuloplasty can be useful for asymptomatic adolescents with critical aortic stenosis
○ May provide short-term benefits for patients who can’t tolerate aortic valve replacement
● Aortic valve replacement is considered for adults with aortic valve area < 0.45 cm2 with left ventricular dysfunction or myocardial ischaemia
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