Other circulation Flashcards
When is flow highest in the left coronary artery and the right coronary artery? Why?
Peak flow in RCA = highest during systole
Peak flow in LCA = highest during diastole
The left ventricle = highly capillarized; when LV contracts during systole >> capillaries get compressed >> increased resistance to flow; thus peak is during diastole when there isn’t resistance to flow
Describe the effect of increased heart rate on left coronary perfusion
If heart rate increases, LV has less filling time therefore flow is decreased (i.e. spending less time in diastole)
Why is the endocardium most at risk for damage if there are perfusion problems? (i.e. explain the relationship between left ventricular pressure, internal pressure and tissue hydrostatic pressure)
When the left ventricle contracts, it exerts pressure on itself (internal pressure) that is equal to the tissue hydrostatic pressure.
What are the factors that influence coronary flow?
Metabolites
Nervous control (symp/parasymp)
Shear stress/Flow-induced vasodilation
Myogenic response
Systolic compression
What are the metabolites that control coronary bloodflow and what is their action?
Adenosine (vasodilation; increases flow/reduces tone)
O2, CO2, H+, K+
How does the sympathetic nervous system regulate coronary blood flow? What about the oarasympathetic system?
Sympathetic: catecholamine binding to alpha receptors (vasoconstriction - increases tone/decreases flow); binding to beta receptors (vasodilation - increases flow/decreases tone)
Parasympathetic: acetylcholine (vasodilation - decreases tone/increases flow)
What is the effect of systolic compression on coronary flow? What about shear stress and the myogenic response?
Systolic compression: constriction = reduced flow b/c increased resistance
Myogenic response: dilation and constriction (depends)
Shear stress/Flow: vasodilation via Nitric Oxide release
What is the relationship between coronary flow and O2 consumption rate?
Directly proportional. A decrease/increase in coronary flow = a decrease/increase in O2 consumption rate by the same factor
T/F: Vasodilator metabolites influence the flow rate but their release is not influenced by flow.
Falsehood. Removal of vasodilators is proportional to the flow rate and vice versa. They influence flow and are influenced by flow.
Describe the autoregulation of coronary blood flow
Even as pressure changes, autoregulation works to keep flow rate constant (so the flow rate can change in either direction depending on the body’s needs)
What’s the difference between active and reactive hyperemia?
Active hyperemia: increased blood flow induced by increased metabolism and increased dilator production
Reactive hyperemia: increased blood flow as a reaction to an ischemic injury (the blood flow/O2 delivery was cutoff and so when flow is returned, the rate goes up sharply)
T/F: Metabolic vasodilation only occurs in the capillaries/tertiary arterioles, which are the highest sight of resistance. How do the coronary arteries dilate? What about the arteries between the coronary arteries and the arterioles?
True.
Large vessels dilate as a result of the myogenic response
Arteries: flow-induced vasodilation
Describe the impact of mild coronary artery stenosis (diffuse, non-flow limiting) on blood flow at rest and during exercise
@ rest: diffuse plaque doesn’t impact arterial resistance and flow
during exercise: arterioles and downstream vessles vasodilate, but plaque prevents flow b/c endothelia are covered by the plaque >> no shear stress >> no flow induced vasodilation
Describe the role of metarterioles and precapillary sphincters in blood flow in the capillary beds
Precapillary sphincters help to control flow in the capillaries
Metarterioles can branch into the capillary beds/link arterioles and venules directly (so they’re just conduits for blood flow)
What’s the difference between hydrostatic and oncotic pressure in the capillaries? How is capillary pressure affected by changes in arterial pressure and venous pressure influence capillary hydrostatic pressure?
Hydrostatic pressure: blood pressure in the capillaries
Oncotic pressure: pressure driven by protein concentration in the plasma
Arterial pressure increases >> Pc increases; arterial resistance increases >> Pc decreases; venous resistance increases >> Pc increases
Major plasma proteins
Albumin
Globulin
Fibrinogen
How do you calculate net fluid movement? What does it mean if Jv is positive? Negative?
Net fluid movement (Jv) = Kf [(Pc - Pi) - (πc -πi)] OR Kf [(Pc+πi) - (Pi+πc)] (no matter which equation, it’s filtration - absorption)
Positive net water movement = filtration
Negative net water movement = absorption
Between the arterial side and venous end, where is Pc the highest/lowest? At which location does absorption/filtration take place?
Pc higher at the arterial end; filtration at that end
Pc lowest at the venous end; filtration at that end
What is the effect of increasing capillary permeability?
(You’d think: a more permeable capillary = increased plasma protein levels = increased capillary oncotic pressure = increased absorption)
But actually (or at least, over time): plasma proteins leak out >> decrease capillary osmotic pressure >> increased filtration out of the capillary
Describe the effect of increasing venous pressure/ venous constriction
Increased venous pressure >> increased capillary hydrostatic pressure >> fluid movement out of the capillary (filtration) and into the interstitial space where it collects and results in edema
Describe the effect of muscle contraction on blood flow in skeletal muscle
Muscle contraction improves venous return b/c with each contraction, blood gets pushed back up to the heart b/c the valves in the veins don’t allow backflow
What is the body’s response to decreased body heat?
Decreased body heat >> hypothalamus promotes sympathetic adrenergic activity >> promotes vasoconstriction >> reduces heat loss
Describe the effect of body heating on cardiac output and blood pressure
Between stroke volume and HR, what’s the biggest contributor to cardiac output?
Increased body heat = increased CO, decreased MAP, decreased mean right atrial pressure
Most of the increase in CO is due to increased HR driven by increased sympathetic nerve activity
Capillary types
Which ones have the highest degree of permeability? What about the lowest?
Continuous capillaries
Fenestrated capillaries
Discontinuous capillaries
Highest permeability: discontinous
Lowest permeability: continuous
Types of intercellular junctions
Tight junctions
Gap junctions
Adherence junctions
How is nitric oxide synthesized and what is the role of NO in vascular smooth muscle? What is the role of Ca2+ and BH4 in NO synthesis? What are the types of NO synthases?
NO = byproduct of the conversion of L arginine to L citrulline by Nitrix Oxide Synthase; Ca2+ activates NO synthase, Bh4 = cofactor
NO promotes vasodilation
NO synthase types:
eNOS: constitutively expressed
iNOS: induced after inflammation or injury
nNOS: neuronal
Describe the synthesis of Prostaglandins and EETs in endothelial cells
What are the downstream effects of Prostaglandins and EETs on vascular smooth ms relaxation?
EETs cause opening of K+ channels (maybe change in Vm from K+ efflux shuts down Ca2+ channels >> decrease in intracellular Ca2+ = decreased contraction)
Prostaglandins activate Adenylyl cyclase >> increased cAMP >> PKA >> MLCK phosphorylation >> no contraction
How do ET1 and TXA2 affect vascular smooth muscle contraction?
They both activate Protein Lipase C >> PIP2 cleavage >> IP3 produced >> binding of IP3 to SR IP3 receptors >> Ca2+ release >> contraction
Outline the movement of lymph fluid in the lymphatic system
Terminal lymphatics >> afferent lymphatics >> lymph nodes >> efferent lymphatics
Characteristics of terminal lymphatics
Characterisctics of collecting lymphatics
What are the features of the lymphangion?
Have striated and non striated cells
Exhibit tonic and phasic contraction; pulsatility: can keep contracting b/c they have an unstable membrane potential
Have valves to propel fluid in one direction
Major nodal regions
Describe the general outline of lymphatic transport
from capillary>> afferent lymph >> lymph node (proteins concentrated here; ultrafiltrate reabsorbed in lymph nodes) >> efferent lymph >> capillary
What are the 2 main lymphatic trunks? Where do they get lymph from and where do they drain?
What are the factors that drive lymph flow?
What is the effect of increasing capillary permeability on lymph flow?
Describe the effect of lymphatic obstruction on lymph flow
What are the causes of lymphedema?
What is the difference between edema and lymphedema?
