Systemic and Pulmonary Hypertensive Disease Flashcards
The most common etiology of systemic hypertension is:
A. Idiopathic processes
B. Renal disease
C. Pheochromocytoma
D. Coarctation of the aorta
A. There are two two types of systemic hypertension: primary and secondary. Primary is the most common and the specific etiology for this condition is idiopathic (90%). Causes of secondary hypertension include renal vascular disease, coarctation of the aorta and pheochromocytoma.
Secondary findings associated with systemic hypertension include all of the following EXCEPT:
A. Left ventricular hypertrophy
B. Left atrial enlargement
C. Increased main pulmonary artery
D. Increased left ventricular mass
C. Several echocardiographic abnormalities are associated with systemic hypertension which include: (1) left ventricular hypertrophy, (2) increased left ventricular mass, (3) left atrial enlargement, (4) left ventricular enlargement (end-stage), (5) mitral annular calcification, (6) aortic dilatation, (7) aortic regurgitation and (8) abnormal left ventricular diastolic function.
The primary pulsed-wave Doppler mitral valve flow pattern associated with systemic hypertension is Grade:
A. I
В. II
C. III
D. IV
A. The prominent diastolic abnormality in systemic hypertension is a relaxation abnormality (Grade I). The Doppler findings include: reduced E/A ratio (< 0.75), prolonged deceleration time (> 220 msec), increased pulmonary vein S wave/D wave ratio (>1), normal pulmonary vein atrial reversal peak velocity (< 35 cm/s), tissue Doppler E’ peak velocity of < 8 cm/s, tissue Doppler E/E’ ratio of < 8 and a dynamic left ventricular outflow tract obstruction (brief dagger-shaped flow pattern located commonly at the level of the left ventricular papillary muscles).
A patient with chronic systemic hypertension presents to the echocardiography laboratory. The following pulsed-wave Doppler mitral inflow data is acquired: E:A ratio 0.66, deceleration time 290 msec, isovolumic relaxation time 132 msec. The Doppler data suggests the diastolic filling grade of Grade:
A. I
В. ІІ
С. III
D. IV
A. Grade I diastolic dysfunction suggest that the primary problem is impaired relaxation with normal filling pressures. Additional parameters would include a pulmonary atrial reversal wave < 35 cm/s, a pulmonary vein atrial reversal duration less than the mitral valve A wave duration, a tissue Doppler of the mitral annulus E’ peak velocity of < 8 cm/s and a tissue Doppler of the mitral annulus E/E’ ratio of < 8.
A late peaking dagger shaped left ventricular outflow tract continuous-wave Doppler flow pattern is obtained in a patient with systemic hypertension. The most likely explanation is:
A. Hypertrophic obstructive cardiomyopathy
B. Left ventricular systolic gradient
C. Discrete subaortic stenosis
D. Coarctation of the aorta
B. In patients with systemic hypertension and left ventricular hypertrophy a dynamic left ventricular systolic gradient may be present. This is seen as a late systolic, usually brief, dagger-shaped continuous-wave Doppler flow pattern.
All of the following may result in secondary pulmonary hypertension EXCEPT:
A. Tricuspid regurgitation
B. Mitral stenosis
C. Left ventricular failure
D. Coronary artery disease
A. Pulmonary hypertension is defined as an increase in the systolic pulmonary artery pressure (> 30 mm Hg). There are several causes of pulmonary hypertension but no matter the disease pulmonary hypertension is a result in the reduction in the caliber of the pulmonary vessels and/or an increase in pulmonary blood flow.
Normal SPAP: < 30 mm Hg
Mild pulmonary hypertension: 30 to 40 mm Hg
Moderate pulmonary hypertension: 40 to 70 mm Hg
Severe pulmonary hypertension: > 70 mm Hg
Eisenmenger physiology: > 120 mm Hg or ≥ systemic pressure
Tricuspid regurgitation may be a result of pulmonary hypertension.
A 44 year old female presents with dyspnea, no history of smoking or cardiac disease and significantly increased pulmonary artery pressures. The most likely explanation is:
A. Grade I diastolic dysfunction
B. Primary pulmonary hypertension
C. Pulmonary regurgitation
D. Tricuspid regurgitation
B. Primary pulmonary hypertension (PPH) is pulmonary hypertension with unexplained etiology. The majority of patients are female (63%), mean age of 36 15 years at the time of diagnosis.
M-mode findings associated with pulmonary hypertension include:
A. Absent or shallow “a” dip of the pulmonary valve
B. Deep “a” dip of the pulmonic valve
C. Paradoxical “a” dip of the pulmonic valve
D. Reverse “a” dip of the pulmonic valve
A. The absence of the “a” wave and mid-systolic notching of the pulmonary valve recorded on M-mode are findings for pulmonary hypertension.
Possible echocardiographic findings for pulmonary hypertension include all of the following EXCEPT:
A. Dilated main pulmonary artery
B. Right ventricular hypertrophy
C. Abdominal aortic aneurysm
D. Tricuspid regurgitation
C. Pulmonary hypertension will often develop secondary to left heart disease (e.g., mitral stenosis). Other echocardiographic findings for pulmonary hypertension include dilated right atrium, dilated right ventricle, “small” left ventricle, paradoxical interventricular septal motion, “flattening” of the interventricular septum during ventricular systole (suggests a right ventricular pressure overload), pulmonary regurgitation and a shortened right ventricular outflow tract acceleration time.
A two-dimensional echocardiographic finding associated with pulmonary hypertension is:
A. Atrial septal aneurysm
B. Flattening of the interventricular septum during ventricular systole
C. Interventricular myocardial infarction
D. Hyperkinetic interventricular septal motion
B. As the right ventricular pressure increases the curve of the interventricular septum changes in ventricular systole. The interventricular septum becomes flatter. Extreme cases of elevated right ventricular systolic pressure may show marked bulging of the interventricular septum toward the left ventricle (D-shaped left ventricle). There will most likely be flattening of the interventricular septum during ventricular diastole as well. The differential diagnosis when there is flattening of the interventricular septum during ventricular systole (and during ventricular diastole) includes pulmonary hypertension, pulmonary embolism, pulmonary stenosis and Eisenmenger’s syndrome.
All of the following may be used to calculate pulmonary artery pressure by cardiac Doppler EXCEPT:
A. Mitral regurgitation
B. Tricuspid regurgitation
C. Pulmonary regurgitation
D. Right ventricular outflow tract acceleration time
A. Tricuspid regurgitation is used in calculating systolic pulmonary artery pressure. Acceleration time allows for calculation of the mean pulmonary artery pressure. Pulmonary regurgitation end-diastolic velocity predicts the pulmonary artery end-diastolic pressure. The peak velocity of pulmonary regurgitation allows for calculation of the mean pulmonary artery pressure.
Mitral regurgitation may be used to calculate left atrial pressure:
Left atrial pressure (mm Hg) = BPs - 4 x (MRV^2max)
BPs, systolic blood pressure;
M, mitral regurgitation;
Vmax, maximum velocity
As the mean pulmonary artery pressure increases, the right ventricular outflow tract acceleration time:
A. Increases
B. Decreases
C. Remains unchanged
D. Depends upon patient age
B. As the mean pulmonary artery pressure increases the acceleration time (measured as the onset of flow to maximum velocity) becomes shorter. The normal acceleration time is ≥ 120 msec. An acceleration time of < 60 msec suggests significant pulmonary hypertension. The mean pulmonary artery may be calculated by the formula:
80 - 0.5 x acceleration time
The acceleration time is influenced by several factors including heart rate and cardiac output and should be used cautiously. Tricuspid regurgitation may be used to determine right ventricular systolic pressure and systolic pulmonary artery pressure. Pulmonary regurgitation may be used to determine the mean pulmonary artery pressure and the pulmonary artery end-diastolic pressure.
