Line 8: |
Line 8: |
| | | |
| ==Pathophysiology== | | ==Pathophysiology== |
| + | The ventricular chambers appear normal or nearly normal, but are restricted in accepting diastolic filling due to the reduced compliance and rigidity of the ventricular walls. |
| + | |
| + | Under normal physiological conditions, diastole can be divided into four phases: |
| + | 1. Isovolumetric relaxation |
| + | 2. Rapid ventricular filling |
| + | 3. Slow ventricular filling (diastasis) |
| + | 4. Atrial contraction |
| + | |
| + | Ventricular filling is influenced by ventricular relaxation, ventricular compliance, atrial contraction and the pressure gradient between the left and right ventricles. The intraventricular pressure gradient is important as it causes an 'untwisting' at the cardiac apex in early diastole; which has a suction effect contributing to ventricular filling. |
| + | |
| + | In RCM, reduced ventricular compliance and distensibility increases the final diastolic pressure, resulting in enlargement of the left atrium. Increased left atrial pressure has a knock-on effect of increased pressure in the pulmonary veins; thus leading to left-sided congestive heart failure (CHF). Tachycardia, associated with icreased sympathetic drive in cardiac dysfunction, contributes to disease progression. Coronary blood flow to the myocardium usually occurs during diastole, tachycardia results in a shorter period of diastole; therefore coronary blood flow is reduced. Reduced myocardial perfusion stimulates myocardial fibrosis, which contributes to rigidity and poor compliance of the ventricles. Finally, the increased atrial pressure and reduced atrial function results in slow blood flow within the atria. This may result in thrombus formation and, in some cases, embolisation of the clot to cause arterial thromboembolism (ATE). |
| + | |
| ==Clinical Signs== | | ==Clinical Signs== |
| ==Diagnosis== | | ==Diagnosis== |