According to kaplan qbank in coarctation pressure tracing in thoraic aorta is greater then abdominal aorta which is due to increase in ANG-II as renal is not adequately perfused ...
but i think pressure in thoracic and abd. aorta should be same as coarctation is proximal to thoracic aorta so...
Increase stroke volume increases pulse pressure. HOW?
If SV is increased then blood pumped by the heart is increased so systolic BP should also increase.. As more blood is now present in aorta so stretch on aorta increases which increases diastolic BP also...so pulse pressure should be same.
Pt. presented with history of sub-sternal pain that radiate to his left shoulder occurs at rest and pain improves when he gets up and move around also improve after taking nitroglycerin..
Likely cause of finding?
1) coronary artery spasm
2) coronary artery thrombosis
3) coronary artery embolism...
1) If total peripheral resistance (TPR) decreases ----- venous return decreases...because of decrease in preload (peripheral pooling of blood)....for example as in case of venodilators which decrease TPR & causing blood to pool in peripheral vessels, thereby decreasing venous return .
I'm a bit confused.
There were 2 Qs in UWorld. One of them meant that the vegetations in Acute bacterial endocarditis caused by S aureus has valvular vegetations made of platelets & fibrin (which I expected to be inflammatory deposit containing bacteria since they embolize to form septic...
Pathoma vids are saying that tunica media is missing in berry aneurysms and Goljan says Internal elastic lamina is missing...looking at histology internal elastic lamina is "A fenestrated layer of elastic tissue that is the outermost part of the intima of an artery. Also called internal elastic...
In goljan pathology he says that fibrinous pericarditis manifests with precordial chest pain which disappears when leaning forward and appears back when leaning back. can someone explain this why this happens?:)
Thanks in advance
Hypokalemia is a risk factor for Torsade de pointes , where as hyperkalemia is not !
Has anyone come across the CONCEPT behind these electrolyte changes causing this type of arrythmia ??
Memorizing them simply just doesn't work :toosad:
I'm a bit confused with the circulation.
Just to clarify I THINK this is how it goes according to FA / Kaplan
1) Umbilical Vein -> Ductus Venosus -> IVC -> Foramen Ovale -> Left Atria -> Left Ventricle ->Aorta. (FA Version)
2) It was mentioned in Kaplan 2010 Umbilical Vein -> Right...