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New page: {{toplink |backcolour = FFADB9 |linkpage =Cardiorespiratory System - Pathology |linktext =Cardiorespiratory System |maplink = Cardiorespiratory System (Content Map) - Pathology |pagetype ...
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|linkpage =Cardiorespiratory System - Pathology
|linktext =Cardiorespiratory System
|maplink = Cardiorespiratory System (Content Map) - Pathology
|pagetype =Pathology
|sublink1=Arterial Disease - Pathology
|subtext1=ARTERIAL DISEASE
|sublink1=Pericardial - Pathology
|subtext1=PERICARDIAL PATHOLOGY
}}
<br>
Cardiac tamponade develops when the intrapericardial pressure increases due to unchecked fluid accumulation within the pericardial sac. As the pericardium is fibrous and inelastic this fluid creates a compression on the heart. Intrapericardial compression leads to diastolic collapse of the right atrium and sometimes the right ventricle, decreased ventricular filling and a resultant decrease in cardiac output. This will lead to arterial hypotension.
Compensatorty mechanisms are activated by the failing heart and include:
*Sympathetic nervous system.
*Renin-angiotensin-aldosterone system.
''Clinical Signs'' are predominantly those of right sided heart failure as the right chambers have thinner walls and so are more greatly affected by the raised intrapericardial pressure.
Clinical signs will include; ascites, hepatomegaly, splenomegaly, hepato-jugular reflux and venous distension due to raised central venous pressure etc.
Heart sounds are muffled or seem distant and a sinus tachycardia may be present.
Arterial pulses will be weak.
'''Pulsus paradoxus''': An exagerrated decline in arterial pulse pressure during inspiration, typical of a pericardial effusion.
|backcolour = FFADB9
|linkpage =Cardiorespiratory System - Pathology
|linktext =Cardiorespiratory System
|maplink = Cardiorespiratory System (Content Map) - Pathology
|pagetype =Pathology
|sublink1=Arterial Disease - Pathology
|subtext1=ARTERIAL DISEASE
|sublink1=Pericardial - Pathology
|subtext1=PERICARDIAL PATHOLOGY
}}
<br>
Cardiac tamponade develops when the intrapericardial pressure increases due to unchecked fluid accumulation within the pericardial sac. As the pericardium is fibrous and inelastic this fluid creates a compression on the heart. Intrapericardial compression leads to diastolic collapse of the right atrium and sometimes the right ventricle, decreased ventricular filling and a resultant decrease in cardiac output. This will lead to arterial hypotension.
Compensatorty mechanisms are activated by the failing heart and include:
*Sympathetic nervous system.
*Renin-angiotensin-aldosterone system.
''Clinical Signs'' are predominantly those of right sided heart failure as the right chambers have thinner walls and so are more greatly affected by the raised intrapericardial pressure.
Clinical signs will include; ascites, hepatomegaly, splenomegaly, hepato-jugular reflux and venous distension due to raised central venous pressure etc.
Heart sounds are muffled or seem distant and a sinus tachycardia may be present.
Arterial pulses will be weak.
'''Pulsus paradoxus''': An exagerrated decline in arterial pulse pressure during inspiration, typical of a pericardial effusion.