Hemodynamics Flashcards
What happens to pressure as we move through circulation?
It decreases. Biggest drop occurs in arterioles.
How do flow, pressure and resistance relate?
Flow = change in hydrostatic pressure / Resistance Q=P/R
How does velocity relate to flow and vessel area?
Flow = velocity X cross sectional area
Poiseuille’s Equation for Vascular Resistance
Blood viscosity increases with…
Increased hematocrit! More force needed to move fluid.
Vessel compliance
Compliance = Volume/Pressure
Low compliance: stiff, difficult to fill
High Compliance: loose, easy to fill (veins)
Compliance is like capacitance, the ability for a vessel to store fluid.
Flow in series
Q1=Q2=Q3
Flow through aorta = flow through all capillaries = flow through all veins
Flow in parallel
Q total = Q1 + Q2 + Q3
Resistance in series
R total = R1 + R2 + R3
If one resistance is much greater than other two, the total resistance is effectively that number.
Resistance in series
1/Rtotal = 1/R1 + 1/R2 + 1/R3
Overall resistance is less than each individual resistance.
Why do capillaries have such low resistance if they have such tiny radii?
Because there are 3 billion of them wired in parallel. The total resistance is less than each individual resistance.
Which vascular section presents the greatest resistance?
Arterioles! Greatest pressure drop equals greatest resistance because flow doesn’t change.
Is blood flow through capillaries slow or fast?
Because v=Q/A, we’d suspect that the flow would be fast, but not so. It’s very slow. Why? Because need to consider total area, or need to divide flow by three billion.
How does the body control blood flow to different organs?
By increasing the resistance in some regions, diverting flow to others. Organs are wired in parallel, so increased resistance at one means reduced resistance at the other!
Why do arterioles have such high resistance?
Not due to the presence of smooth muscles, more due to the fact that they’re not much bigger than capillaries, and there aren’t nearly as many.
MAP
Mean arterial pressure = Cardiac output x Total peripheral resistance.
This is a causal relationship. Changes in cardiac output and total peripheral resistance cause changes in MAP.
MAP relationship to diastolic and systolic BP
MAP = 2/3 DP + 1/3 SP
Because diastole is longer than systole.
Baroreceptors
Located in carotid sinus and aortic arch. When they stretch, they send more impulses to the medulla to regulate BP.
Three phases of the baroreceptor response
Direct response that changes MAP. The reflex response, which attempts to return MAP to where it was initially. A new steady state is achieved.
Direct Response After Hemorrhage
Decreased blood volume leads to reduced ventricular filling. Reduced ventricular filling leads to reduced stroke volume. Reduced stroke volume causes decreased cardiac output, which decreases MAP.
Cardiac Output = ?
CO = HR X Stroke Volume
The Reflex Response after hemorrhage
Decreased MAP due to decreased cardiac output causes reduced baroreceptor firing to medulla. This causes increased sympathetic output to SA node, ventricles, arterioles, veins, and decreased parasympathetic output to SA node.
Increased sympathetic output to SA node increases HR, to ventricles increases contractility,
How does increased sympathetic output and decreased parasympathetic output affect hr on a molecular level?
Increased Symp: Beta adrenergic activation of cAMP which increases If.
Decreased Para: Decreased activation of Ik,Ach by BG subunit of mAChR.
How does increased sympathetic output to ventricles increase contractility on a molecular level?
Increased B adrenergic activation causes PKA activation, which P’s phospholamban to increase amount of Ca in SR and which P’s L type Ca channels to increase amount of Ca in cell.
How does increased sympathetic output to arterioles increase total peripheral resistance on a molecular level?
Activation of alpha 1 receptors by NE causes the production of IP3, which causes SR Ca2+ release and smooth muscle contraction. This occurs slowly.
Venoconstriction
Reduces venous compliance, which increases ventricular filling (preload).
Atrial Stretch Receptors
As blood volume increases in atria, they stretch and ANP is released into bloodstream.
ANP
Atrial Natriuretic Peptide, which dilates blood vessels to decrease TPR and MAP. Also blocks renal sodium reabsorption to cause increased Na secretion, which will decrease blood volume.
Where are central chemoreceptors located? What do they do?
Located in the carotid body and the aortic arch. Respond to decreases in O2. Causes vasoconstriction and increased breathing.
Long term regulation of blood pressure
Accomplished by the renin-angiotensin-aldosterone system.
RAAS
Decreased pressure in kidneys causes release of renin. Renin cleaves angiotensinogen to angiotensin I, which is cleaved by angiotensin converting enzyme (ACE) to angiotensin II, which causes 1) increased aldosterone, and 2) vasoconstriction.
Increased aldosterone causes Na reabsorption in kidney and increases blood volume.
How does AngII cause vaso constriction?
By activating the release of Ca through an IP3 Gq pathway.
What are the long term effects of angiotensin II
Can reset baroreceptors. When AngII is present, higher heart rate and higher pressure.
