Valve area (cm2)
Maximal aortic velocity (m/s)
Mean pressure gradient (mmHg)
Mild
>1.5
<3.0
<25
Moderate
1.0–1.5
3.0–4.0
25–40
Severe
0.6–0.9
>4.0
>40
Critical
<0.6
>4.0
>70
- 4.
What are the different grades for mitral regurgitation? (Table 5.2) [1]
Table 5.2
Different grades for mitral regurgitation
Mild
Moderate
Severe
Angiographic grade
1+
2+
3+–4+
Color Doppler jet area
Small, central jet <4 cm2 or <20% of left atrial size
Signs of MR greater than mild, but not severe
Vena contracta width >0.7 cm2 with large central jet (area >40% of left atrium) or with a wall-impinging jet swirling in left atrium
Doppler Vena contracta width (cm)
<0.3
0.3 – 0.69
≥0.7
Regurgitant volume (ml/beat)
<30
30-59
≥60
Regurgitant fraction (%)
<30
30-49
≥50
Regurgitant orifice area (cm2)
<0.2
0.2–0.39
≥0.4
Left atrial size
Normal, unless other causes of left atrial dilation
Normal or dilated
Dilated, except acute MR
Left ventricular size
Normal, unless other causes of left ventricular dilation
Normal or dilated
Dilated, except acute MR
Mitral leaflets or support apparatus
Normal or abnormal
Normal of abnormal
Abnormal/flail leaflet, ruptured papillary muscle
- 5.
What is the natural progression of aortic stenosis?
Aortic stenosis is the most common valvular lesion in the United States. Aortic stenosis is classically associated with a prolonged asymptomatic period followed by rapid development of symptoms. The three primary symptoms are angina, syncope and dyspnea on exertion (symptom of heart failure). Without intervention, these correlate with an average life expectancy of two to five years.
Risk factors for developing aortic stenosis include: increased age, male gender, dyslipidemia, diabetes, hypertension, smoking, renal insufficiency, or abnormal valve substrate. In high-risk patients, persistent inflammation, shear stress and pro-calcific stimuli ultimately result in valvular obstruction, decreased left ventricular ejection fraction and onset of symptoms. [2].
- 6.
What is the natural progression of mitral regurgitation
Mitral regurgitation most commonly develops gradually because the left atrium and left ventricle are initially able to compensate for regurgitant flow. The left atrium accommodates the regurgitant volume by dilating, while the left ventricle undergoes remodeling and hypertrophy to maintain adequate forward flow. However, with an increasing regurgitant volume, the myocardial demand exceeds supply and results in decreased forward stroke volume, reduced cardiac output and subsequently decompensated heart failure.
In instances of acute mitral regurgitation, there is an abrupt increase in left atrial pressure without any time for left atrial or ventricular compensation; thus, the patient often develops acute pulmonary edema, decompensated heart failure, and cardiogenic shock.
- 7.
How does aortic stenosis change the physiology of the heart?
The primary physiologic change in aortic stenosis is left ventricular outflow obstruction. Left ventricular outflow obstruction leads to an increased left ventricular systolic pressure and a prolonged ejection time in order to maintain cardiac output. To meet demand, the left ventricle undergoes concentric hypertrophy. With the reduction in LV compliance, the stroke volume becomes fixed. Myocardial oxygen demand increases in the presence of a hypertrophied left ventricle; however, coronary oxygen supply can be limited secondary due to the myocardial hypertrophy. The result is left ventricular dysfunction, myocardial ischemia and, without intervention, left ventricular failure.
- 8.
How does mitral regurgitation change the physiology of the heart?Related posts:
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