L20 Special Circulation: Coronary & Skeletal Flashcards
Coronary Circulation
From the aorta, the right and left coronary branch off after the semilunar valves.
Right CA - wraps around behind and gives the Posterior Descending Branch
Left CA - gives the Left Anterior Descending Branch & the Circumflex branch
How does cardiac tissue pressure determine coronary blood flow?
A huge amount of pressure is created by LV contraction. This pressure is so much that it compresses the LCA when the LV contracts and squeezes out the blood – the blood in the LCA shoots up and joins the blood being ejected from the LV into the aorta. Only after diastole (when the LV is relaxed and not creating pressure) that the LCA opens up and fills with the blood that pools back onto the aortic valve when it shuts. The elastic recoil of the aorta also helps push blood into the CAs.
Since DP is the pressure created when the aortic valve closes, the DP determines the filling of the CAs and a LOW DP would impede CA filling
How does LV EDP affect endo/epicardial coronary blood flow?
Ventricular DP is the pressure “felt” on the endocardial surface when blood fills into the LV. Thus, the endocardial vessels experience a higher P and would be compressed more. Given this natural difference in P, the endocardial vessels normally dilate more to maintain an equal BF.
In ABNORMAL conditions, when EDP is much higher, the endocardial vessels cannot dilate enough to overcome the pressure difference and this reduces coronary BF.
When DP is very low (the container’s amount of “fullness”), the capillaries in the endocardium have such a low blood volume that they become flaccid and get crushed much more easily.
~~ultimately due to compression by DP in ventricle, or tissue compression during contraction
Neural vs. Metabolic regulation of coronary BF
Neural - not as important
Metabolic - VERY IMPORTANT
Neural:
Sympathetic = very few alpha receptors bc you don’t really want to constrict the heart vessels; ß1 receptors on the myocardium and pacemakers causes VASODILATION; Some ß2 receptors are present to vasodilate
Parasympathetic = not much innervation to the heart, but vagus can induce dilation
Metabolic Factors - THE PRIMARY REGULATORS
BF and metabolism are directly related
More O² consumption = more metabolism = more vasodilation = less resistance = more BF
Heart uses: fatty acids and carbs for E. Fatty acids require the most O2 to break down.
The heart is flow limited; this means that the heart can only get more O2 by increasing the amount of blood that flows through it; it cannot do extracting tricks to get more O2 out of the same amount of blood.
Myocardial Oxygen Supply
Suppliers of the Heart’s O2 demand:
The diastolic P - this determines if the coronaries are filling
Are the coronaries dilating and adjusting resistance appropriately?
The O2 carrying capacity of the blood in the coronaries
Myocardial O2 Demand
Demand:
Afterload - how hard does the heart have to work to expel blood is DIRECTLY related to how much O2 it needs
Heart Rate - higher HR = more ATP = more O2
Contractility - if the heart has good contractility it uses more Ca2+ and more O2 to create and contract the crossbridges
Not having enough of the supply can cause ischemia. The *healthy *heart will never demand too much O2.
Coronary Steal
REST:
A clogged artery vasodilates to allow BF to pass the clogged area. The non-clogged vessel is normally constricted.
EXERCISE:
As soon as exercise starts and large scale vasodilation starts, the non-clogged vessel dilates and now has a path of lesser resistance for the blood to travel down. Therefore, the blood is stolen from the lesioned area and fast tracked down the newly vasodilated healthy vessel.
Metabolic regulation of Skeletal Muscle
Active Hyperemia - vasodilating when BF increases through an area
Sk.M. is a balance between constrictors (rest) and dilators (exercise)
Mechanical regulation of Skeletal muscle circulation
When muscles contract, tissue P increases and vessels are compressed.
In exercise, vessels are contracting, relaxing, contracting, relaxing, etc. This pattern results in an overall increase in BF
(Vasodilation = reduced resistance = exercise ; Constriction = increased resistance = rest)
Neural regulation of Skeletal muscle circulation
ALMOST COMPLETELY CONTROLLED BY ADRENERGICS
NE binds to alpha receptors –> constriction (what is happening at rest)
Sympathetic cholinergics (the weird exceptions) use Ach on muscarinic receptors –> dilation
*Epinephrine: *at HIGH concentrations –> acts on alpha receptors to CONSTRICT
at LOW concentrations --\> acts on ß2 receptors to DILATE
