Coronary and Pulmonary Circulation Flashcards
extravascular pressure is greater in which- epicardial coronary or subendocardial arterial plexus?
subendocardial plexus= more sensitive to damage
-even greater on L side
Ohms law and coronary blood flow:
Change in pressure (Inlet-outlet)/Resistance
SAME FOR pulmonary flow
Resistance is whose law? What is the main factor we consider?
Poiseuilles law
inversely related to radium^4
(also length and viscosity of fluid)
SAME FOR pulmonary flow
Regulators of coronary vascular tone:
1) Systolic compression
2) Myogenic mechanisms
3) Metabolic factors
4) autonomic control
When is coronary flow lowest?
End of diastole - end of isovolumetric contraction = A LOT OF TENSION IN THE VENTRICLE!
When is coronary flow intermediate level?
throughout most of systole
LV is maximally perfused during:
diastole!
LV is minimally perfused during:
systole with lowest point at the end of isovolumetric contraction
How to supply the heart with more O2?
Must inc blood flow - the heart already pulls almost all the O2 out of the blood it gets so that is not an option - must inc flow (dilate vessels!)
Mechanisms to inc O2 demand for heart:
O2 supply:
- inc coronary conductance (opposite of resistance) –> vasodiilation
- inc diastolic perfusion pressure
- inc arterial O2 concentration - long term= more Hb
O2 demand increases when?
Inc HR
- inc contractility
- inc wall tension
What is myogenic regulation:
its autoregulation that no matter the pressure (range of pressures) blood flow is actively maintained at constant level
What is coronary reserve:
the difference between passive movement (capacity of pipes) due to pressure and the autoreg curve (active maintenance of tension in vessel)
Example of when coronary reserve is reduced?
-disease can impair dilatory potential of vessels (plaque, atherosclerosis?) –> reduced blood flow fora given perfusion pressure
Metabolic regulation of coronary blood flow is measured/stimulated how in the heart??
non-pathological hypoxia ==> tells the system to crank out some ATP + adenosine byproducts (adenosine also vasodilate the vessels)
Sympathetics regulatino of blood flow:
PHASE 1
-stimulation causes transient vasoconstriction via direct action of NE on alpha receptors
PHASE 2
-then vasodilation - indirect effect bc METABOLIC regulation stimulated = hypoxia –> ATP –> adenosine vasodilation stuff
Special features of pulmonary vessels?What does this do for us?
- high elastic content
- low smooth muscle content
allows for phasic distention to accomodate entire CO each cycle
–>opposite of autoreg (pressure changes with respect to change in flow)
(LOW PRESSURE< LOW RESISTANCE< VASCULAR DIFFERENCES compared to systemic circulation)
Blood flow through Zone 1 Lungs:
-low capillary hydrostatic pressure because we are going up hill
Blood flow through Zone 3 Lungs:
-High capillary hydrostatis pressure
Why do crackles occur in Zone 3 first?
inc capillary hydrostatic pressure compared to other zones bc it is easy for blood to follow gravity to the bottom of lung = lymph drainage of excess fluid = crackles
Ventialation is highest?
at the apex
Perfusion is highest?
at the base
V/Q at the apex is? at the base?
apex: large number
base: small number
Passive mechanisms for regulation of pulmonary blood flow:
1) recruitment - adding more pipes - opening previously closed capillaries
2) distention - making the pipes bigger - accomodation of inc blood volume
Active mechanisms for regulation of pulmonary blood flow:
1) hypoxic vasoconstriction
- caused by airway obstruction, high altitude, acute lung damage, COPD
- close area off by constricting adjacent blood vessels to divert blood to better areas
- “Decrease wasted ventilation”
2) other metabolites (limited in normal function)
What happens with long term hypoxic vasoconstriction:
hypoxic stimulus for a while will cause hypertrophy of the smooth muscle in vessels = even more resistance to flow = inc pulmonary pressure = RV hypertorphy = RV dilation, valvular issues and evenually failure
