Archive for January, 2016
Dizzines , giddiness , light headedness , fear of fall or true fall (Syncope) are the most common symptoms beyond middle age .They usually end up with consulting physicians , neurologists and cardiologists .Cervical disc is commonly blamed for this.While all these symptoms can be a manifestation of cervical disc , true syncope seems to be rare with cervical spinal disorder.
There is a fundamental ignorance here. We are not yet clear whether giddiness /dizziness is neural or vascular .(Or combinations of both ) in cervical spinal disease.
Many of the patients experience momentary unsteadiness and feel like falling but very rarely end up in a fall or syncope.By definition syncope requires global transient hypoperfusion of brain to trigger a fall .
Cervical canal carries only the vertebral artery .Both internal carotids are no where near the spine. So, however severe the vascular compromise within the cervical canal , syncope is unlikely as anterior cerebral circulation compensates at the level of circle of Willis. Is that the correct way of reasoning ? Unilateral vertebral compromise rarely matters as other side takes care.It is very unlikely both vertebral artery get compromised by cervical spinal spurs simultaneously.
How many seconds of vascular compromise is required to produce syncope ?
Brain seems to be a funny and sensitive organ .In erect posture it is very sensitive. It reacts in a fraction of time for any transient reduction of blood flow.The same cardiac events which can cause symptoms of impending syncope in erect posture is quiet comfortably tackled in recumbent posture .
In erect posture , blood pressure need to much higher to get it pumped above the heart against the gravity. Though , it seems absolute blood pressure and cerebral perfusion that matters, there is something more we are missing. The brain-stem -vestibular system perceives differently when a recumbent person develop cerebral ischemia than when he is erect . The reflex circuit that activates on/off switch for abrubt loss generalised muscular tone is not yet been identified .
It is a biologically heartening irony that syncope is a natural counter mechanism by which the organism assumes instant recumbent position to maintain perfusion of brain .A fall promptly does this.(Ofcourse with a risk of Injury )
We think more than 3 second pause will initiate a syncope circuit .But it is not a fixed number. Some can tolerate up to 5sec or even more especially in lying posture.
Syncope , as such in isolated cervical spondylosis is rare even though it can potentially interfere with the vertebro basilar system .Why the vascular compromise almost always fall short of syncope and end up with just momentry unsteadiness is not clear.
Further queries to be addressed
Is dizziness, giddiness , presyncope are vascular or neural event?
Can vertigo occur with cervival spine disease ?
Posted in acute coronary syndrome, atherosclerosis, platelet function, tagged platelet adhesion and aggrgation and fatty meal briyani, platelet stickyness and dietery fat, platlet anf fat ldl and triglycerides, tgl mediated platlet aggregation on January 31, 2016 | Leave a Comment »
Posted in admixture lesions in cyanotic heart disease, cardiology -congenital heart disease, Tetrology of Fallot, tagged admixture lesions in congenital heart disease, can left to right shunt cause cyanosis ?, mechansim of cyanosis, mechansim of cyanotic heart disease, what is admixture lesion on January 19, 2016 | Leave a Comment »
What are the mechanisms of cyanosis in cyanotic heart disease ?
Most of my fellows have difficulty in answering this question. (It is not the lack of knowledge though !) In my view ,cyanosis can occur , by six different modes
- Reduced pulmonary blood flow with some form of anatomical obstruction in RVOT with a communication between ventricles (TOF physiology ) , atria or both
- Reduced pulmonary flow with obstructive pulmonary vasculature (Eisenmenger physiology )
- Wrong way origin ( RV to Aorta/LV to Pulmonary artery ) : Transposition physiology
- Simple mixing of arterial and venous blood channels within the atria ,ventricle or great vessel without RVOT obstruction .This, in fact can causes increased pulmonary blood flow (Technically left to right shunt ) and still there is cyanosis (These are called as Admixture lesions ) It is also to be noted some of the admixture lesions (Truncus, DORV,etc ) the mixing takes place only during systole , while TAPVC,Common atrium, Tricuspid atresia* admixture is more complete as it happens during entire cardiac cycle.
- Isolated Right to left shunt are very rare ( Pulmonary AV fistula , SVC to LA )
- Complex combination of first 4 (Like bi-directional shunting , TGA combines , AV canal defect , with varying degree of pulmonary obstructive disease) Note : TOF and Eisenmenger are physiologically mimic each other , the only difference is site of resistance to pulmonary flow. RVOT vs Lung vasculature )
* Essentially Atrial admixture is more complete than when it happens at ventricular or great vessel level
For advanced readers only
Now, is it possible for “Net” left to right shunt to result in cyanosis ?
Yes*.Very much possible. The bulk of this group is referred to as admixture lesions with certain caveats.There should be an obligatory mixing without contribution from RVOT obstruction or raised PVR( *Please note theoretically admixture can either be right to left or left to right shunt )
All pure admixture lesions are in fact net left to right shunts. (TAPVC, Single ventricle , Common atrium , Common AV canal ,Truncus, ) This is the group we have been traditionally calling cyanosis with increased pulmonary flow.
Its may also to be noted with surprise some admixture lesions often has less intense cyanosis than other forms as long as pulmonary blood flow is normal and the lung does its job perfectly .
*Please note Isolated classical left to right shunts , ASD, VSD, PDA can never cause significant cyanosis unless there is reversal of flow .However ,many Eisenmenger physiology show net Left to right shunting only ( 1.2-1.5 : 1 or so ) but with a definite right to left component .What we call as typically bi-directional shunt .
How can cyanosis be minimal even in some cases of single ventricle ?
- Even though there is single ventricle , there can be preferential (favorable) streaming of right heart blood flow without gross mixing .
- As discussed before good uninterrupted pulmonary blood flow will make the cyanosis less intense .
Is single ventricle with PS admixture lesion or TOF physiology ?
Though single ventricle in isolation is an admixture lesion, when it has associated RVOT obstruction it ceases to be admixture by definition as mixing is augmented by the obstruction rather than by simple mixing.The complexity could be understood in certain situations where admixture lesions like common AV canal go for raised PVR .Here the various quantum of contribution to cyanosis is mind boggling. (Original admixture, augmented by RVOT resistance, differential mixing at atrial and ventricular level , hypoxia at lung level due micro pulmonary AV fistulas in grade 4 heath Edwards etc )
Can TOF behave like an admixture lesions ?
Technically Yes.If the RVOT obstruction is minimal , (What was called then as pink Fallot ) We haven’t understood this entity properly for so long.Atleast I was baffled to read when J.K Perloff mentioned in his book during my DM fellowship days, that TOF can manifest with predominant left to right shunt with little or absent cyanosis.
The aortic override in TOF facilitated by large malaligned VSD make it a sort of admixture situation as RVOT resistance is too little to offer any resistance, (rather it welcomes more blood from left side ! ) So , should we call it simple VSD physiology , admixture physiology or just acyanotic forms of TOF ?)
Though admixure lesions are discussed separately , bulk of them actually represent cyanosis with increased pulmonary blood flow situations.
The net pulmonary blood flow is much more important than the quantum of admixture in determining the degree cyanosis
Finally , one should appreciate there can be combination admixture lesions with obstructive RVOT components . (Tricupid atresia+Pulmonary stenois )
An excellent review article on this rare topic of admixture physiology
- Jaganmohan A Tharakan Admixture lesions in congenital cyanotic heart disease Ann Pediatr Cardiol. 2011 Jan-Jun; 4(1): 53–59.