Week 9 the heart and blood pressure II

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Last updated 8:04 PM on 6/13/26
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34 Terms

1
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systolic and diastolic blood pressure:

  • troughs are diastolic, peaks are systolic

  • ventricles have larger range than arteries, ventricle go almsot to 0 arteries don’t

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pulse pressure

systolic pressure minus diastolic pressure

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mean arterial pressure

  • diastolic pressure + 1/3 (pulse pressure)

  • MAP = 80 + 40/3 = 93.3

  • should be between 70-100

  • when MAP is too low (<60) - organs don't get enough oxygen, syncope shock

  • when MAP is too high - the heart has to work too hard, muscle will enlarge. Increase oxygen demand by the heart, vascular injury, end organ damage, stroke

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pulse pressure should be:

40mmHg, this is typically 30-40 in a healthy adult

  • extremely low like 25mmHg or less: low stroke volume, weak ventricular contractions

  • pulse pressure > 60: predictor of heart attacks or other cardiovascular disease

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arterial baroflex system is:

key regulator of MAP

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factors that influence mean arterial pressure:

  • effectiveness of the heart as a pump/cardiac output (heart rate, stroke volume), fast autonomic

  • resistance of the system to blood flow (diameter of the arterioles), fast, autonomic, local control mechanisms

  • blood volume determines by fluid intake, fluid loss (passive, regulated at kidneys), slower, hormonal regulation

  • relative distribution of blood between arterial and venous blood vessels (diamter of veins), fast autonomic

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heart valve opening:

A: aortic valve opens

B: aortic valve closes

C: mitral valve close

D: mitral valve open

E: end diastolic volume

F: end systolic

volume

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what determines mean arterial pressure?

mean arterial pressure is proportional to your cardiac output times the resistance of your arterioles

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Frank Starling Law

  • The relationship between end-diastolic volume (EDV) and stroke volume (SV) (amount of blood flowing back into the heart before systole determines the stroke volume)

  • As a larger volume of blood flows into the ventricle, the blood will stretch the walls of the heart, causing a greater expansion during diastole, which in turn increases the force of the contraction and thus the quantity of blood that is pumped into the aorta during systole

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frank-starling law graph

  • Factors that increase cardiac contractility will lead to an upward and leftward shift of the curve.

  • In contrast, factors that decrease cardiac contractility will lead to a downward and rightward shift of the curve

  • Stronger contraction = more blood out, less left behind and vice versa

<ul><li><p>Factors that increase cardiac contractility will lead to an upward and leftward shift of the curve.</p></li><li><p>In contrast, factors that decrease cardiac contractility will lead to a downward and rightward shift of the curve</p></li><li><p>Stronger contraction = more blood out, less left behind and vice versa</p></li></ul><p></p>
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the frank-starling mechanism in vertebrate cardiac myocytes

The cellular mechanisms underlying the Frank–Starling response include an increase

in myofilament sensitivity for Ca2+, decreased myofilament lattice spacing and

increased thin filament cooperativity.

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sympathetic nervous system regulation of heart rate

Pathway

  • Preganglionic neurons originate in the thoracic spinal cord.

  • Postganglionic neurons release norepinephrine (NE) onto the heart.

  • NE binds β₁-adrenergic receptors on cardiac cells.

Results

  • SA node fires action potentials more frequently.

  • AV node conducts signals faster.

  • Ventricles contract more strongly.

Overall effects:

  • ↑ Heart rate (positive chronotropy)

  • ↑ Conduction velocity (positive dromotropy)

  • ↑ Contractility (positive inotropy)

Cellular Mechanism

β₁ receptor activation increases cAMP, which:

  • Opens more pacemaker ion channels.

  • Increases Ca²⁺ entry.

  • Causes the SA node membrane potential to reach threshold faster.

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parasympathetic nervous system regulation of heart rate

Effect: Decreases heart rate.

Pathway

  • Mainly through the vagus nerve (cranial nerve X).

  • Postganglionic neurons release acetylcholine (ACh).

  • ACh binds M2 muscarinic receptors.

Results

  • SA node fires more slowly.

  • AV node conduction slows.

Overall effects:

  • ↓ Heart rate (negative chronotropy)

  • ↓ Conduction velocity (negative dromotropy)

Cellular Mechanism

M2 receptor activation:

  • Decreases cAMP.

  • Opens K⁺ channels.

  • Hyperpolarizes pacemaker cells.

  • Slows the rate of spontaneous depolarization.

As a result, it takes longer to reach threshold for the next heartbeat.

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where blood is needed most to least:

  • lungs

  • brain

  • heart

  • liver and digestive tract

  • kidneys

  • skeletal muscle

  • skin

  • bone and other tissues

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myogenic auto-regulation - regulation of blood flow at the tissue level

activation of a mechanoreceptor depolarizes muscle, contraction

  • Myogenic autoregulation is the ability of certain blood vessels (especially arterioles) to automatically adjust their diameter in response to changes in blood pressure, helping keep blood flow relatively constant.

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paracrine: active and reactive hyperemia - regulation of blood flow at the tissue level

  • some vasoactive paracrines are related to inflammation

  • Paracrine regulation of blood flow refers to local chemical signals released by tissues that act on nearby blood vessels to adjust blood flow according to metabolic demand.

  • decrease O2, increase CO2, NO lead to vasodilation

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active hyperemia

Definition: Increased blood flow to a tissue when its metabolic activity increases.

What happens?

When a tissue becomes more active (e.g., exercising skeletal muscle):

  • O₂ consumption increases.

  • CO₂ production increases.

  • H⁺, K⁺, adenosine, lactate, and other metabolites accumulate.

These metabolites act as paracrine signals that cause arterioles to dilate.

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reactive hyperemia

Definition: A temporary increase in blood flow after blood supply has been blocked and then restored.

What happens?

  1. Blood flow is reduced or occluded.

  2. Tissue continues metabolizing.

  3. Vasodilatory metabolites accumulate.

  4. Oxygen levels fall.

  5. When the blockage is removed, arterioles are already strongly dilated.

Result

  • Blood flow temporarily rises above normal.

  • Excess flow repays the "oxygen debt."

  • Accumulated metabolites are washed out.

  • Blood flow gradually returns to baseline.

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sympathetic nervous system controls most:

vascular smooth muscle

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APs in vascular smooth muscle

  • more firing - more contraction

  • less firing - less contraction

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the microcirculation

1) every cells is within 0.1µm of a capillary

2) capillary density is related to the metabolic activity of the tissue (even in bones)

3) capillaries are the only “open” part of the vasculature system

4) an adult human has 50,000 miles of capillaries'

5) capillaries are made of a single layer of flattened endothelial cells

6) diameter of a capillary is 1 red blood cell, many types of white blood cells are too big

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arteriole

  • controllable diameter

  • smooth muscles

  • capillaries

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precapillary sphincters

  • sympathetic control

  • regulate blood flow at the tissue level

  • neuron firing tells them to contract

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metarterioles

  • can act as bypass channels

  • there is also the arteriovenous bypass, bypasses capillaries if sphincters are closed

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sphincters relaxed vs contracted

more blood flow when relaxed, less blood flow when contracted

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velocity of blood flow:

velocity is reduced with larger cross-sectional areas

ex: capillaries have least velocity and largest cross-sectional area

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exchange of material takes place at the capillaries:

  • most capillaries are continuous capillaries with leaky junctions

  • endothelial cell junctions allow water and small dissolved solutes to pass

  • transcytosis: brings proteins and macromolecules across endothelium, some vesicles may fuse to create temporary channels

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fenestrated capillaries

  • large pores

  • eg posterior pituitary, OT and AVP and kidney

  • help transport material as well as junctions and transcytosis

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pressure does what through arterial system?

decreases

  • arteries high pressure

  • capillaries/veinous low pressure

<p>decreases</p><ul><li><p>arteries high pressure</p></li><li><p>capillaries/veinous low pressure</p></li></ul><p></p>
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bulk flow of fluid:

  • arteriole to net filtration to lymph vessels and net absorption, out to venous circulation and venule

  • bulk flow is driven by hydrostatic and osmotic pressure (Starling forces)

  • filtration - flow from blood into tissue. absorption back into venous side, a function of pressure

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bulk flow in systemic capillaries

  • hydrostatic pressure forces fluid out of the capillary

  • colloid osmotic pressure of proteins with the capillary pulls fluid into the capillary

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filtration:

  • arteriel end net filtration pressure = +10mmHg

  • fluid exits capillary since hydrostatic pressure is GREATER than blood colloidal osmotic pressure

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no net movement

  • mid capillary net filtration pressure = 0mmHg

  • bc hydrostatic and blood colloidal osmotic pressure are equal

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reabsorption

  • venous and net filtration pressure = -7mmHg

  • fluid re-enters capillary since capillary hydrostatic pressure is less than blood colloidal osmotic pressure (25mmHg)