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Circulation Flashcards

1
Q

What are the 3 main components of circulatory systems?

A
  • pump or propulsive structures (ie. heart)
  • system of tubes, channels, or spaces
  • fluid that circulates through system (ie. blood)
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2
Q

What are the 3 types of pumps?

A
  • chambered hearts
  • skeletal muscle
  • pulsating blood vessels
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3
Q

How do chambered heart pumps work?

A
  • contractile chambers
  • blood moves into muscular wall through vein
  • muscular wall contracts
  • one-way valves ensure unidirectional blood flow out of chamber through artery into circulatory system
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4
Q

How do skeletal muscle (external) pumps work?

A
  • muscle mass contracts, compressing blood in vessel to generate pressure, which forces blood unidirectionally through one-way valve
  • no specifically designed chamber
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5
Q

How do pulsating blood vessel pumps work?

A
  • peristalsis: rhythmic contractions of vessel wall (contractile tissue) pumps blood by elevating hydrostatic pressure, which forces blood to move in intended direction of flow
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6
Q

What are the 4 types of fluid?

A
  • blood
  • hemolymph
  • interstitial fluid
  • lymph*
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7
Q

What is blood?

A

fluid that circulates within vessel of closed circulatory system

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8
Q

What is hemolymph?

A

fluid that circulates in open circulatory system

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9
Q

What is interstitial fluid?

A

extracellular fluid (between cells) that directly bathes tissues

  • composition similar to plasma
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10
Q

What is lymph?

A

fluid that circulates in lymphatic system

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11
Q

What is the lymphatic system?

A

secondary circulatory system of vertebrates that carries fluid (lymph) that filtered out of vessel

  • capillaries are not perfectly impermeable
  • pressure that drives blood forces some fluid out across membrane into interstitial fluid → lymph ducts → lymph vessels
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12
Q

What is an open circulatory system?

A

circulatory fluid comes in direct contact with tissues in spaces called sinuses

  • circulating fluid mixes with interstitial fluid
  • heart pumps hemolymph to one end of animal, fluid enters big open space (hemocoel), and eventually gets drawn back into venous system to return to heart
  • no control of how fluid returns to heart – just mixes the contents to make sure nutrients are distributed throughout the body
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13
Q

What is the tracheal system?

A
  • brings air to within 2-3 cells of every cell in the body
  • O2 brought into system, CO2 removed
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14
Q

Does the hemocoel play a role in gas exchange?

A

no – more about nutrients, waste products

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15
Q

What is a closed circulatory system?

A

circulatory fluid remains within vessels and doesn’t come in direct contact with tissues

  • circulating fluid is distinct from interstitial fluid
  • efficient way of circulating fluid throughout body, but molecules must diffuse across vessel wall
  • heart pumps blood through circulatory system into capillary bed (high surface area) – everything diffuses across membranes, and blood remains in circulatory system
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16
Q

What happens at the capillaries? (3)

A

diffusion of molecules between blood and interstitial fluid occurs

  • gas exchange (O2 in, CO2 out)
  • nutrient delivery from blood
  • lymph is generated (which then needs to be removed)
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17
Q

Why did the circulatory system first evolve, and how did it change?

A
  • first evolved to transport nutrients to body cells
  • very early began to serve respiratory function – get O2 to metabolizing tissues, and CO2 away from tissues
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18
Q

How did closed circulatory systems evolve? What did this do?

A

evolved independently in jawed vertebrates, cephalopods, and annelids

  • increased blood pressure and flow
  • and therefore increased control of blood distribution
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19
Q

What did closed circulatory system evolve in combination with?

A

with specialized oxygen carrier molecules

  • high metabolic rates
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20
Q

How does the circulatory system fit into O2 delivery?

A

O2 cascade – framework for all vertebrate animals

  • external convection
  • diffusion
  • internal convection
  • diffusion
  • ATP production
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21
Q

Describe the steps of the O2 cascade.

A
  • EXTERNAL CONVECTION moves air into lungs to obtain O2 from external medium
  • DIFFUSION of O2 across barrier and into circulatory system – to quickly and fully saturate respiratory pigment with O2
  • INTERNAL CONVECTION – circulatory system pumps blood around circuit of tubes to get blood to where and when it is needed
  • DIFFUSION to rapidly unload O2 from blood to mitochondria of tissues
  • ATP PRODUCTION
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22
Q

What is convection important for?

A

for getting medium as close as possible to site where it needs to diffuse, which greatly reduces time constraints

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23
Q

All activities (locomotion, digestion, reproduction, etc.) ultimately require O2. What are the two ways of providing it?

A
  • heart pumps more blood per unit time (higher cardiac output) with activity intensity
  • tissues extract more O2 from capillaries with activity intensity (CaO2 remains constant, CvO2 decreases)
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24
Q

What is the equation for O2 uptake?

A

MO2 = Q(CaO2-CvO2)

  • CaO2: content of O2 in arterial blood
  • CvO2: content of O2 in venous blood
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25
Q

What happens to blood saturation when you increase activity intensity under resting conditions?

A

high arterial saturation, will extract ~50% of O2 in blood

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26
Q

What is the goal (in terms of blood saturation) when you increase exercise intensity?

A

goal is still to saturate blood completely

  • usually possible
  • can extract more O2 from venous system with each pumping of blood to satisfy metabolic demand
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27
Q

What happens when you double O2 extraction and increase CO by 4-fold?

A

increase metabolic rate by 8-fold

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28
Q

What happens to blood O2 content at altitude?

A
  • breathing O2 levels that are much lower than at sea level
  • total CaO2 reduced, requires drop in CvO2 to maintain same metabolic rate – this puts limits on maximum metabolic rate
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29
Q

How is O2 unloading based on supply and demand?

A

high metabolic activity (mitochondria doing more work) decreases PO2 because O2 is consumed, which increases partial pressure gradient to increase O2 movement from venous blood to tissue

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30
Q

What are the two types of closed circulatory systems?

A
  • single-circuit (most fishes)
  • double-circuit (all birds and mammals)
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31
Q

Describe the circulatory plan of vertebrates.

A
  • blood leaves heart in arteries
  • arteries branch out into arteries with smaller diameter
  • small arteries branch out into arterioles within tissues
  • blood flows from arterioles into capillaries
  • capillaries coalesce to form venules
  • venules coalesce to form veins
  • blood flows to heart in veins
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32
Q

What is the central lumen?

A

interior of a vessel (tube) through which blood flows

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33
Q

What are the 3 layers of the complex wall that surrounds the central lumen?

A
  • tunica intima
  • tunica media
  • tunica externa
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34
Q

What is the tunica intima?

A

internal lining

  • smooth, epithelial cells (vascular endothelium) that are in direct contact with plasma moving through central lumen
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35
Q

What is the tunica media?

A

middle layer

  • smooth muscle (if needed)
  • elastic connective tissue (that allows for expansion and contraction of muscle)
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36
Q

What is the tunica externa?

A

outermost layer

  • collagen (provides structural support)
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37
Q

Why does the thickness of the wall vary among vessels?

A
  • arteries are more muscular than veins because they need to be able to handle high blood pressure and transmit force evenly
  • venous end is low pressure (after passing through high resistance capillaries) and acts as reservoir to return blood back to heart
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38
Q

Which layers do venules lack?

A
  • tunica media
  • tunica intima
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39
Q

Which layers do arterioles lack?

A
  • tunica externa
  • tunica intima
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40
Q

What layers do capillaries lack?

A
  • tunica media
  • tunica externa
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41
Q

What are the 3 types of capillaries?

A
  • continuous capillaries
  • fenestrated capillaries
  • sinusoidal capillaries
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42
Q

What are continuous capillaries? Where are they located?

A
  • in skin and muscle
  • cells held together by tight junctions – not permeable
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43
Q

What are fenestrated capillaries? Where are they located?

A
  • in kidneys, endocrine organs, and intestine
  • cells contain pores – designed to be leaky so fluids (such as water and salts) can move in and out to some degree
  • specialized for exchange
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44
Q

What are sinusoidal capillaries? Where are they located?

A
  • in liver and bone marrow
  • few tight junctions
  • most porous for exchange of large proteins
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45
Q

What are capillaries specialized based on?

A

based on needs and type of exchange required of the tissue

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46
Q

What is tank treading?

A
  • capillary diameter is slightly smaller than RBC diameter
  • RBCs need to squeeze through capillary (tank treading), which mixes contents of RBC and promotes diffusion
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47
Q

What are accessory hearts?

A

hearts in the tail of some water-breathing fish that helps pump blood back to heart

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48
Q

What is pressure?

A

potential energy to send blood anywhere in body that needs

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49
Q

What is the law of bulk flow?

A

Q = ΔP/R

  • Q: flow
  • ΔP: pressure drop
  • R: resistance
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50
Q

What is the equation for resistance?

A

R = 8Lη / πr^4

  • L: length of tube
  • η: viscosity of fluid
  • r: radius of tube (vasoconstriction, vasodilation)
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51
Q

What is Poiseuille’s equation?

A

Q = ΔPπr^4 / 8Lη

more detailed version of law of bulk flow

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52
Q

Like electrical resistors, blood vessels can be arranged in series or parallel.

A

resistors in series: RT = R1 + R2 …

  • fish capillary beds

resistors in parallel: 1/RT = 1/R1 + 1/R2 …

  • overcomes problems with resistance

because of law of conservation of mass, flow through each segment of the system must be equal if R is the same

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53
Q

What is flow (Q)?

A

volume of fluid transferred per unit time

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54
Q

What is the equation for blood velocity?

A

blood velocity = Q/A

  • A: cross-sectional area of channels
  • velocity of flow is inversely related to total cross-sectional area
  • large total cross-sectional area of capillaries → slow velocity → more time for diffusion
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55
Q

Why do you want low velocity in capillaries?

A

velocity drops dramatically where total cross-sectional area of capillaries is high

  • great for delivering O2, taking up CO2
  • RBC is squeezing through capillary – tank treading to mix its contents

(total area increases in smaller vessels)

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56
Q

What are the two different types of myocardium?

A
  • compact myocardium
  • spongy myocardium
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57
Q

What is compact myocardium?

A
  • tightly packed cells arranged in regular pattern
  • can generate lots of force
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58
Q

What is spongy myocardium?

A
  • meshwork of loosely connected cells
  • bathed by blood
  • allows lots of blood to move in and around muscle
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59
Q

Are there coronary arteries in compact myocardium?

A
  • coronary artery moves through myocardium – perfusing, providing lots of O2, and removing lots of CO2
  • specialized, completely new/evolved arterial network
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60
Q

Are there coronary arteries in spongy myocardium?

A
  • lacks coronary vessels
  • all O2 has to be extracted from blood that is perfusing through heart
  • this evolved first in fish
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61
Q

Where does compact myocardium receive O2 from?

A

from coronary arteries

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62
Q

Where does spongy myocardium receive O2 from?

A

from blood flowing through (perfusing) heart

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63
Q

What are the 4 main parts of the complex walls of vertebrate hearts?

A
  • pericardium
  • epicardium
  • myocardium
  • endocardium
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64
Q

What is the pericardium?

A
  • sac of connective tissue that surrounds heart
  • outer (parietal) and inner (visceral) layers, with space between them containing lubricating fluid
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65
Q

What is the epicardium?

A
  • outer layer of heart, continuous with visceral pericardium
  • contains nerves that regulate heart and coronary arteries that bring oxygenated blood to myocardium
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66
Q

What is the myocardium?

A
  • layer of heart muscle cells (cardiomyocytes)
  • contractile tissue that pumps blood
  • extremely oxidative – has high O2 demand
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67
Q

What is endocardium?

A
  • innermost layer of connective tissue covered by epithelial cells (endothelium)
  • direct interface between blood and muscle
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68
Q

What is the cardiac cycle?

A

pumping action of heart – two phases

  • systole: contraction – blood is forced out into circulation
  • diastole: relaxation – blood enters heart
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69
Q

What are the 3 types of pacemakers?

A
  • neurogenic
  • myogenic
  • artificial
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70
Q

What is a neurogenic pacemaker?

A
  • rhythm generated in neurons
  • continuous pace
  • found in some invertebrates
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71
Q

What is a myogenic pacemaker?

A
  • rhythm generated in myocytes
  • cardiomyocytes (muscle cells) produce spontaneous rhythmic depolarizations – cells are electrically coupled via gap junctions to ensure coordinated contractions (AP passes directly from cell to cell)
  • do not require nerve signal
  • in vertebrates and some invertebrates
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72
Q

What is an artificial pacemaker?

A

rhythm generated by device

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73
Q

Cell membranes are polarized. What is the resting (stable) membrane potential in vertebrates?

A
  • -60 mV to -110 mV inside
  • inside is always relative to outside
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74
Q

What is a resting membrane potential?

A

created by ATPases working against selectively permeable ion channels (ie. Na+, K+, Ca2+, Cl-), resulting in ionic gradients across cell membrane

  • ATPases pump 3 Na+ for 2 K+ to generate electrical potential
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75
Q

What do electrochemical gradients do?

A
  • is the ‘battery’ for life – electrical potential energy for many of cell’s activities
  • only time it disappears, and everything comes into equilibrium, is at death
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76
Q

Why are some cells (ie. neurons, muscles) excitable?

A

because ion channel permeabilities can change briefly

  • such voltage-gated ion channels in muscle cells can create AP, which triggers muscle contraction
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77
Q

Do pacemaker cells have stable resting membrane potentials? Why?

A

no – unstable

  • due to slow decrease in K+ conductance and opening of funny channels (Na+ channels)
  • reduces outflow of K+
  • increases probability of Na+ inflow
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78
Q

Describe the steps of how vertebrate pacemaker APs are generated.

A
  1. cell gradually depolarizes to threshold (-40 mV)
  2. opens voltage-gated channels
  • permeability for Na+ increases – enters cell and makes inside less negative
  1. initiates spike (AP)
  • AP due to voltage-gated Ca2+ channels
  • permeability for Ca2+ increases – enters cell and makes inside less negative
  • changes in permeability of different channels in different regions of AP drives change in membrane potential
  1. cell repolarizes
  • K+ channels initiate repolarization phase
  • permeability for K+ increases – leaves cell and makes inside more negative
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79
Q

What are the relative concentrations of Na+, Ca2+, and K+ inside and outside of cells?

A
  • Na+ high outside of cell, low inside
  • Ca2+ high outside of cell, low inside
  • K+ low outside of cell, high inside
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80
Q

What are the major differences between action potentials and pacemaker potentials?

A
  • in most nerve function, there is stimulus that alters membrane permeability, which results in Na+ influx to generate AP, K+ recovery and hyperpolarization, then flat threshold until next stimulus is received
  • but in AP there is never a stable resting membrane – it is always drifting to ensure heart is beating at some constant rate
  • but we can change heart rate
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81
Q

How does sympathetic stimulation affect heart rate?

A

increases rate of pacemaker potentials

  • increases rate of depolarization (channels opening)
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82
Q

How does parasympathetic stimulation affect heart rate?

A

decreases rate of pacemaker potentials

  • decreases rate of depolarization (channels opening)
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83
Q

Describe the steps of how sympathetic stimulation increases heart rate.

A
  1. norepinephrine (noradrenaline) released from sympathetic neurons OR epinephrine (adrenaline) released from adrenal medulla bind to beta receptors of autorhythmic cells
  • stimulates cAMP release
  • results in protein kinase
  1. more Na+ and Ca2+ channels open, increasing influx of both ions
  2. rate of depolarization and frequency of APs increase
  3. heart rate increases
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84
Q

Describe the steps of how parasympathetic stimulation decreases heart rate.

A
  1. acetylcholine released from parasympathetic neurons binds to muscarinic receptors of autorhythmic cells
  2. more K+ channels open, and Ca2+ channels close
  • efflux of K+ increases
  • influx of Ca2+ decreases
  1. pacemaker cell hyperpolarizes
  2. time for depolarization increases, therefore frequency of APs decreases
  3. heart rate decreases
85
Q

What are the two ways that depolarization travels through the heart?

A
  • specialized conducting pathways
  • directly between cardiomyocytes
86
Q

APs are generated through the heart by a single autorhythmic event. Describe how this occurs.

A
  • membrane potential of autorhythmic cell – one impulse that sets up entire cardiac contraction cycle
  • autorhythmic cell sends signal to cardiomyocytes
  • cardiomyocytes have different type of AP that occurs, leading to coordinated contraction of heart
  • AP is propagated from cardiomyocyte to cardiomyocyte via intercalated disks with gap junctions (electrically coupled)
87
Q

Specialized Conducting Pathways

What are modified cardiomyocytes? What do they do?

A
  • cells with elongated, pale appearance
  • lack contractile proteins
  • spread AP rapidly throughout myocardium – SA node sets up initial AP, which is then propagated and transmitted through pathway that allows for rhythmic depolarizations of the heart
88
Q

Directly Between Cardiomyocytes

How do depolarizations travel between cardiomyocytes?

A
  • myocardial muscle cells are branched, have single nucleus
  • cardiomyocytes are electrically connected via intercalated disks with gap junctions
  • electrical signals can pass directly from cell to cell
  • crucial that propagation is coordinated – need AP to be delivered to appropriate myocytes at appropriate time to get a nice predictable contraction
89
Q

Describe the steps of excitation-contraction coupling (how AP results in cardiomyocyte contraction).

A
  1. AP enters cardiomyocyte from adjacent cell
  2. voltage-gated Ca2+ channels open, and Ca2+ enters cell
  3. entry of Ca2+ triggers release of Ca2+ from sarcoplasmic reticulum
  • released to proximity of actin and myosin (contractile tissues of cardiomyocytes)
  • most Ca2+ comes from SR
  1. Ca2+ ions bind to troponin to initiate contraction – via activating sliding of actin and myosin together
  2. relaxation occurs when Ca2+ unbinds from troponin
  3. Ca2+ is pumped back into SR for storage
  4. Ca2+ is exchanged with Na+
  5. Na+ gradient is maintained by Na+-K+-ATPase
90
Q

Describe the propagation of the electrical signal (conducting pathway) throughout the mammalian heart from the SA node.

A
  1. SA node (autorhythmic cell) depolarizes, and depolarization spreads rapidly via internodal pathway
  • forceful contraction at apex of heart forces blood up through aortic system
  1. AV node delays signal
  • depolarization spreads through atria via gap junctions, and causes atria to contract
  • transmission to ventricles is delayed so atria can contract
  1. depolarization spreads rapidly through bundles of His and Purkinje fibres
  2. depolarization spreads upward through ventricle, causing ventricle to contract
91
Q

How do APs in cardiomyocytes differ from those in skeletal muscle?

A

has plateau phase instead of repolarizing quickly like APs do

  • plateau phase: extended depolarization that lasts as long as ventricular contraction
  • largely a function of changes in K+ and Ca2+ permeability
  • caused by Ca2+ entry via L-type channel
  • influx of Ca2+ into cell results in sustained depolarization
  • prevents tetanus
92
Q

Do APs in the heart all have the same shape?

A

no – have different shapes for different reasons

  • different regions of the system have different channel types that open at different electrical thresholds and densities
  • SA node dominates AV node
  • bundle of His and ventricular cardiomyocyte have plateau phase
93
Q

Describe the steps of a normal skeletal muscle contraction.

A
  • AP stimulates muscle contraction
  • Ca2+ is released, binds to troponin, and induces muscle contraction
  • one AP results in large contraction and relaxation
94
Q

Describe the contraction/recovery cycle of skeletal muscle under normal conditions. What happens if you exercise, or if there is a problem?

A
  • under normal conditions, AP occurs at some rate, and there is full contraction and recovery before next AP
  • if running, APs occur more frequently, and there is not complete relaxation
  • if there is problem (tetanus) or want sustained muscle contraction (ie. flexed arm hang), want continuous contraction and muscle does not have time to relax
95
Q

Describe the contraction/recovery cycle of cardiac muscle under normal conditions. What happens if you exercise?

A
  • heart has built-in time delay (plateau phase) – takes time before AP can recover, and next signal can be delivered
  • when resting, there is AP that stimulates cardiac contraction and recovery of nerve and muscle before next AP is generated
  • when exercising maximally, AP is at some high rate, but can still have complete recovery of heart because of plateau phase – delay prevents heart from being in sustained contracted state
96
Q

What is an autoarrhythmia?

A

fibrillation of heart

  • APs generated more quickly than muscle can recover
97
Q

What is an electrocardiogram (ECG or EKG)?

A

composite recording of APs in cardiac muscle

98
Q

What are the 3 main parts of an ECG?

A
  • P wave: atrial depolarization
  • QRS complex: ventricular depolarization
  • T wave: ventricular repolarization
99
Q

What kind of information do ECGs indicate?

A

indicates change in electrical pulse

  • opposed to directional (positive vs. negative)
100
Q

How do hearts function as an integrated organ?

A
  • electrical and mechanical events are correlated
  • changes in pressure and volume of chambers
  • blood flow through chambers
  • heart sounds – opening and closing of valve
101
Q

What initiates contractile events?

A

electrical events

102
Q

Describe how the EKG waves correspond with pressure changes in the heart.

A

pressure increases in left atrium and ventricle before P-wave

  • due to passive filling from venous pressure and venous return

P-wave initiates atrial contraction and atrial BP peaks

QRS-complex initiates ventricular contraction and ventricular BP peaks – atrial relaxation occurs at same time

  • ventricles contract quite a bit after initial signal because it takes time for Ca2+ to be released, bind to troponin to contract, be released from troponin, and absorbed back into SR
  • pressure falls in left ventricle
  • ventricular BP first exceeds atrial BP, then aortic diastolic BP

T-wave is initiation of ventricular relaxation

  • ventricular BP first falls below aortic BP, then below atrial BP

energy stored in aorta is slowly released

103
Q

What is end-systolic volume (ESV)?

A

volume of heart at end of contraction

104
Q

What is end-diastolic volume (EDV)?

A

volume of heart before contraction

  • heart is relaxed, filling
  • some atrial pressure generated
105
Q

What is the equation for cardiac stroke volume?

A

cardiac stroke volume = EDV - ESV

  • adult human = 60 ml per heartbeat
106
Q

Does a heartbeat fully empty the human ventricle?

A

no – during resting conditions

no – during exercise

  • EDV likely will not change much because it is at full as it can be (but may change slightly based on venous pressure)
  • ESV can decrease because force of contraction will empty that ventricle more
107
Q

Why does blood aortic blood pressure decrease during diastole?

A

more blood is transported away, to the body

108
Q

What is cardiac output? What is the equation?

A

volume of blood pumped per unit time

CO = HR x SV

  • heart rate (HR): rate of contraction (beats per minute)
  • stroke volume (SV): volume of blood pumped with each beat
109
Q

What can cardiac output be modified by? (2)

A
  • regulating heart rate
  • stroke volume
110
Q

How does heart rate modify cardiac output?

A

modulated by autonomic nerves and adrenal medulla

  • decreased HR through parasympathetic system (bradycardia)
  • increased HR through sympathetic system (tachycardia)
111
Q

How does stroke volume modify cardiac output?

A

modulated by various nervous, hormonal, and physical factors

  • adrenergic control
  • Frank-Starling effect (passive control) and length-force relationships of skeletal muscle

lots of control over how much blood is pumped with each heartbeat – dependent on pressure relationships, hormonal relationships, and neural relationships

112
Q

How is stroke volume controlled by adrenergic control?

A

nervous and endocrine systems can cause heart to contract more forcefully and pump more blood with each beat

  • pathway promotes muscle contraction (activated by) Ca2+, and increases rate of Ca2+ removal
  • increased force of contraction
  • increased conditions for relaxation
  • this will increase stroke volume (degree of emptying of ventricle)
113
Q

Describe the steps of how adrenergic control can control stroke volume.

A
  1. binding of norepinephrine or epinephrine changes shape of beta-1 adrenergic receptor, which activates associated G protein
  2. G protein subunit activates adenylate cyclase
  3. adenylate cyclase catalyzes conversion of ATP to cAMP
  4. cAMP activates protein kinase A
  5. protein kinase phosphorylates L-type Ca2+ channels, allowing Ca2+ to enter cell, which stimulates contraction
  6. protein kinase phosphorylates Ca2+ channels on sarcoplasmic reticulum, allowing Ca2+ to move to cytoplasm, which stimulates contraction
  7. protein kinase phosphorylates myosin, stimulating contraction
  8. protein kinase phosphorylates sarcoplasmic Ca2+ ATPase, speeding removal of Ca2+ from cytoplasm during relaxation, which decreases relaxation time
114
Q

What is the Frank-Starling effect (passive control of stroke volume)?

A

increased EDV results in more forceful contraction and increased SV

  • high venous BP → high filling of chambers during diastole → more blood that needs to be pumped out
  • increasing venous return increases volume of blood pumped with each heartbeat – partly a direct effect of stretching ventricular wall (length-tension relationship)
115
Q

Frank-Starling Effect

What is the length-tension relationships for muscles?

A

filling (greater EDV) causes stretching of muscle, which potentiates more forceful contraction – chamber is fuller, therefore has to work harder to empty

  • as sarcomeres are stretched (more filling), more force can be generated up to some point, then muscle tissue starts to tear and fall apart
116
Q

How does the heart autoregulate?

A

heart automatically compensates for increases in volume of blood returning to heart

  • more blood comes in → more forceful contraction to make sure it can remove the blood
117
Q

What can affect the position of cardiac muscle length-tension relationships?

A

length of sympathetic activity

  • increased sympathetic activity increases stroke volume because force of contraction is greater
  • decreased sympathetic activity decreases stroke volume for a given diastolic volume
118
Q

What vessels control blood distribution?

A

arterioles arranged in parallel

  • can alter blood flow to various organs by changing resistance by vasoconstriction and vasodilation
119
Q

What are the 3 factors that control vasoconstriction and vasodilation?

A
  • autoregulation
  • intrinsic factors
  • extrinsic factors
120
Q

What is autoregulation?

A

direct response of arteriole smooth muscle (to blood moving to that capillary system)

121
Q

What are intrinsic factors?

A

metabolic state of tissue

  • if muscle is metabolically active, it consumes O2 and produces CO2 – these factors directly influence blood flow
122
Q

What are extrinsic factors?

A

nervous and endocrine systems

123
Q

Why is a parallel arrangement of arterioles better than an in-series arrangement?

A

parallel arrangement allows lots of control over blood

  • blood flow in series (tissue after tissue) has lots of resistance, therefore not much fine control over tissue-specific blood flow
124
Q

What sets blood distribution?

A

tissue metabolic needs

  • blood can be redistributed as needed
125
Q

What % of resting blood flow goes to the brain?

A

14%

  • brain is highly metabolically active – under all conditions, must keep blood flow there
126
Q

What % of resting blood flow goes to the heart?

A

4%

  • heart pumps 100% of blood, but only 4% perfuses tissues that drive pump
127
Q

What % of resting blood flow goes to the liver and digestive tract?

A

27%

  • liver is highly metabolically active – purification system for body
128
Q

What % of resting blood flow goes to the kidneys?

A

20%

  • kidney is important part of homeostasis – need to make sure that ammonia and nitrogenous waste excretion is accomplished
  • kidney is major organ in maintaining blood volume, which feeds into pressure
129
Q

What % of resting blood flow goes to skeletal muscle?

A

21%

130
Q

What % of resting blood flow goes to the skin?

A

5%

131
Q

What % of resting blood flow goes to bone and other tissue?

A

9%

132
Q

What is the main rule for vasoconstriction and vasodilation alteration of tissue-specific blood flow?

A

total flow out must equal total flow in

  • increasing flow in one vessel must be compensated by decreasing flow in another vessel
133
Q

What do pre-capillary sphincters do?

A

contraction of pre-capillary sphincters reduces blood flow to capillary bed

134
Q

How can you reduce the amount of blood vessel to a tissue?

A
  • under some conditions, all vessels will be relatively dilated and relaxed
  • blood flow is driven by pressure of arterial system and diameter of respective vessels

can reduce the amount of blood vessel to a tissue by:

  • reducing blood flow to that arteriole
  • influencing capillary perfusion within arteriole by closing sphincters
135
Q

What is myogenic autoregulation of flow?

A

some smooth muscle cells in arterioles are sensitive to stretch and contract when blood pressure increases

  • acts as negative feedback loop – want to maintain similar blood flow
  • prevents excessive flow of blood into tissue
136
Q

How is increased metabolic activity of tissue a signal of blood requirement?

A
  • increases metabolism
  • decreases O2 – being consumed
  • increases CO2 – being produced
137
Q

What are smooth muscle cells in arterioles sensitive to?

A

extracellular fluid (plasma of blood + interstitial fluid around cells) conditions

  • levels of metabolites alter vasoconstriction/vasodilation
  • blood flow is matched to metabolic requirements
138
Q

What happens when tissue metabolic rate increases?

A
  • decreases O2, increases CO2, increases waste
  • arteriolar smooth muscle sense changes in ECF (plasma of blood + interstitial fluid around cells) conditions
  • VASODILATION
  • decrease resistance
  • increase blood flow
  • increase O2 delivery, increase CO2 removal, increase waste removal
  • increase tissue O2, decrease tissue CO2, decrease tissue waste
  • negative feedback loop – conditions sensed by arteriolar smooth muscle
139
Q

Neural and Endocrine Control of Flow

What does norepinephrine do?

A

(from sympathetic neurons) causes vasoconstriction

140
Q

Neural and Endocrine Control of Flow

What is sympathetic tone?

A

some level of vasoconstriction or vasodilation due to some level/concentration of norepinephrine and epinephrine existing all the time in circulatory system

  • allows for flexibility of control
141
Q

Neural and Endocrine Control of Flow

What does decreased sympathetic tone cause?

A

vasodilation

142
Q

Neural and Endocrine Control of Flow

What are the other 3 hormones that affect vascular smooth muscle?

A

(released under specific conditions, and interact with levels of already-circulating hormones)

  • vasopressin (ADH)
  • angiotensin II
  • atrial natriuretic peptide (ANP)
143
Q

Neural and Endocrine Control of Flow

What is vasopressin (ADH)?

A

hormone from posterior pituitary that causes generalized vasoconstriction

144
Q

Neural and Endocrine Control of Flow

What is angiotensin II?

A

hormone produced in response to decreased blood pressure that causes generalized vasoconstriction

145
Q

Neural and Endocrine Control of Flow

What is atrial natriuretic peptide (ANP)?

A

hormone produced in response to increased blood pressure that promotes generalized vasodilation

146
Q

What is blood pressure?

A

potential to drive blood through entire circulatory system

  • further away from heart → lower pressure (or greater decrease in pressure)
147
Q

How does blood velocity change throughout vertebrate circulatory systems?

A

velocity of blood highest in arteries, lowest in capillaries, and intermediate in veins

148
Q

How does blood pressure change throughout vertebrate circulatory systems?

A
  • blood pressure decreases as blood moves through system
  • blood pressure in left ventricle changes with systole and diastole
  • pressure and pulse decrease in arterioles due to high resistance
149
Q

In vertebrate circulatory systems, why is there a large decrease in the degree of blood pressure oscillations in the arteries compared to the left ventricle?

A
  • greater area for pressure to be distributed (?)
  • autoregulation (?)

venous vs. arterial system have different amounts of collagen, connective tissue, and muscle

  • arterial system has great ability for dampening due to its elasticity
  • large pressure pulse allows expansion then contraction as blood moves away to dampen oscillations
150
Q

How do arteries act a pressure dampeners?

A

aorta acts as pressure reservoir

  • high elasticity of vessel wall – expands during systole, elastic recoil during diastole
  • stores energy in contraction, recovers energy as pressure falls
  • dampens pressure fluctuations
151
Q

What would occur if the arterial system was very rigid and had no ability to dampen?

A

pressure oscillation seen in left ventricle would be transmitted far downstream through circulatory system

  • all those blood vessels will be exposed to very large oscillation in pressure, which would be a challenge
152
Q

What do veins act as?

A

volume reservoir

  • veins have thin, compliant walls
  • small increases in blood pressure lead to large changes in volume
  • in mammals, veins hold more than 60% of blood
153
Q

What is vein volume (and venous return) controlled by?

A

sympathetic nerves

154
Q

What is venomotor tone?

A

tone of venous system that ensures there is decent blood pressure to fill the heart during relaxation just prior to contraction

155
Q

How does blood volume in the arterial and venous systems differ as blood pressure in the artery or vein increases? Why?

A

there is some increase in volume in arterial system, but very large increase in volume in venous system

  • at a given pressure, venous system volume is much greater than arterial system because it has less constrictive characteristics (less muscle and resistance to stretching)
  • important for dealing with blood flowing back to heart
156
Q

Is blood in veins under high or low pressure?

A

low pressure

157
Q

What are the two pumps that assist in moving blood back to the heart?

A
  • skeletal muscle: contraction (shortening and thickening) of muscle squeezes vein – but contraction cannot be sustained or blood flow will be shut down completely
  • respiratory pumps: pressure changes in thoracic cavity during ventilation
158
Q

Are there valves in veins?

A

yes – ensures unidirectional blood flow

159
Q

What is the equation for mean arterial pressure (MAP)?

A

MAP = CO x TPR

160
Q

What is the diving reflex?

A

diving animals modify CO (massive bradycardia to reduce overall blood flow during dive) and increase TPR to maintain constant MAP

161
Q

What is constant MAP important for?

A

important for tissues that need blood flow – need to dilate or constrict vessels downstream of that to get nice control of blood that goes to respective tissues

162
Q

Factors Affecting MAP

What influences cardiac output?

A

heart rate

  • parasympathetic nervous system (acetylcholine) DECREASES heart rate, therefore DECREASES cardiac output
  • sympathetic nervous system and epinephrine INCREASES heart rate, therefore INCREASES cardiac output

stroke volume

  • sympathetic nervous system and epinephrine INCREASES stroke volume and force of contraction, therefore INCREASES cardiac output
  • increased end-diastolic volume (EDV) INCREASES stroke volume – Frank Starling effect, where increasing pressure increases ejection, which factors into stroke volume
163
Q

Factors Affecting MAP

Increasing EDV increases stroke volume, and therefore cardiac output. What increases EDV?

A

increased venous return, which is caused by:

  • increased blood volume
  • increased respiratory pump activity
  • increased skeletal muscle activity
164
Q

Factors Affecting MAP

What influences TPR?

A

arteriolar tone

  • metabolites and paracrines
  • sympathetic nervous system and epinephrine (causes constriction)
  • vasopressin and angiotensin II (causes constriction)

blood viscosity

  • increased number of RBCs to increase hematocrit increases blood viscosity, which increases TPR (ie. at altitude)
165
Q

Factors Affecting MAP

Vasopressin and angiotensin II influences arteriolar tone by causing constriction, and therefore increases TPR. What other role do these hormones play?

A

influence blood flow to kidneys

  • which influences salt and water balance in circulatory system
  • which influences salt and water balance between interstitial fluid and extracellular fluid of blood
  • which influences blood volume

recall that increased blood volume increases venous return, which increases EDV, which increases stroke volume, and thus increases cardiac output to alter MAP

166
Q

What is the baroreceptor reflex?

A

baroreceptors interpret MAP changes and send nerve signals to medulla oblongata (cardiovascular control center) to regulate MAP

167
Q

What are baroreceptors?

A

stretch-sensitive mechanoreceptors in walls of many major blood vessels, especially carotid arteries and aorta

168
Q

Baroreceptor Reflex

What occurs when MAP increases?

A
  • increases baroreceptor firing
  • stimulates afferent neurons
  • influences cardiovascular control centre (medulla)
  • decreases sympathetic output
  • decreases norepinephrine release, which eventually decreases MAP

(recall: under normal conditions, there is some sympathetic tone)

169
Q

Baroreceptor Reflex

How does reduced norepinephrine release result in a decrease in MAP?

A
  • vasodilation of arteriolar smooth muscle decreases peripheral resistance, which decreases MAP
  • decreased force of contraction of ventricular myocardium decreases cardiac output, which decreases MAP
  • SA node influenced and decreased heart rate decreases cardiac output, which decreases MAP

(negative feedback increases MAP)

170
Q

How do kidneys help maintain blood volume?

A
  • increases in blood volume leads to increase in blood pressure, and vice versa
  • kidneys excrete or retain water to adjust blood volume (and pressure)
171
Q

What is blood volume crucial for?

A

maintaining MAP, CO, etc.

172
Q

If MAP increases, how do kidneys help maintain blood volume?

A
  • increase excretion of Na+ and H2O
  • decreases plasma volume
  • decreases blood volume
  • decreases venous pressure
  • decreases EDV
  • decreases cardiac muscle contractility (Frank-Starling effect)
  • decreases stroke volume
  • decreases cardiac output
    (negative feedback increases arterial pressure)
173
Q

What is the basis for net filtration pressure (NFP)?

A
  • interstitial fluid on other side of capillary membrane
  • blood pressure (from high to low) drives blood flow through capillary
  • tendency for hydrostatic pressure (gravitational effects resulting in high pressure) to drive fluid/water out of capillary
  • tendency for osmotic pressure to drive water in opposite direction (high osmolality in fluid draws water because of high osmotic pressure)
  • net flux of water is balance between hydrostatic pressure and osmotic pressure
174
Q

Why is blood pressure in the lungs low?

A

so fluid does not get filtered out of capillaries and into lung

  • edema
  • would drown in body fluid
175
Q

What is the Starling principle?

A

NFP = (Pcap - Pif) - (π cap - π if)

  • Pcap: hydrostatic pressure of blood in capillary
  • Pif: hydrostatic pressure of interstitial fluid
  • π cap: osmotic pressure in capillary
  • π if: osmotic pressure interstitial fluid

above are the dominant forces that potentially drive water across membranes

  • total net outcome determines direction of water movement
176
Q

What is hydrostatic pressure?

A
  • blood pressure
  • pressure of column of fluid due to gravity
177
Q

What is osmotic pressure?

A

pressure due to osmotic tensions – arises due to salts and proteins in solution

178
Q

How does blood pressure change from arterial end to venous end of capillaries?

A

blood pressure at arterial and venous ends of capillaries have very different pressures

  • blood pressure falls as blood moves through capillary due to resistance
179
Q

How does osmotic pressure change from arterial end to venous end of capillaries?

A

stays basically constant

180
Q

Is there net filtration or reabsorption at the arterial end of capillaries? Why?

A

net filtration

  • Pcap > πcap
  • force to move water from inside capillary to interstitial space is greater than osmotic pressure to retain that fluid
181
Q

Is there net filtration or reabsorption at the venous end of capillaries? Why?

A

net reabsorption

  • πcap > Pcap
  • water is absorbed into capillary system
182
Q

Is there ever a point in a capillary when Pcap = πcap?

A

yes

183
Q

Why is there microcirculation in and out of capillaries?

A

due to differences in hydrostatic and osmotic pressures

  • water movement between cells helps with mixing, diffusion, and provide cells with glucose/etc. that is in interstitial space
184
Q

What does the lymphatic system do?

A

collects excess filtered fluid and returns it to circulatory system

185
Q

What do lymph nodes do?

A

filter lymph to remove pathogens – has some immunological role

186
Q

What are lymphocytes?

A

cells in lymph nodes that kill pathogens

187
Q

Do lymphatic veins and ducts have valves?

A

yes – contain (unidirectional) valves to prevent backflow

188
Q

What drives lymphatic return?

A
  • no heart pumping
  • net water pressures and body movements (muscular pumps that force fluids through primary circulatory system) drive lymphatic return
189
Q

What is edema?

A

accumulation of interstitial fluid (swelling)

190
Q

What is elephantiasis?

A

parasite physically blocks nodes and prevents fluid from making it back to circulatory system

191
Q

What is the equation for the pressure difference between two points (hydrostatic pressure)?

A

ΔP = ρgΔh

  • ρ: density of fluid
  • g: acceleration due to gravity
  • Δh: height of fluid column
192
Q

(blood pressures we have discussed up to now within circulatory system are largely in absence of gravitational effects)

A

–

193
Q

Body Position and Blood Pressure

How does venous pressure at every height differ from arterial pressure? Why?

A

venous pressures at each height is about 100 mmHg lower than arterial pressures to permit blood flow

194
Q

Body Position and Blood Pressure

Are there gravitational effects when lying down?

A

very little

  • pressure at every body position is similar
195
Q

Body Position and Blood Pressure

Are there gravitational effects when standing up?

A

yes

  • body is a column of water
  • low in column (closer to feet) → higher pressure
  • high in column (above heart) → lower pressure because need to fight against gravity
196
Q

Body Position and Blood Pressure

At any height, should venous pressure or arterial pressure be higher? Why?

A

venous pressure at any height must be lower than arterial pressure to ensure blood flow through respective capillary system

  • blood is pumped from arterial to venous side of every tissue in body
  • below heart, arterial blood supply pumps blood through that capillary bed – by the time blood reaches venous system, pressure has decreased dramatically because there is lots of resistance to that blood flow
  • (in diagram: venous pressure is 90 mmHg lower than arterial pressure at any position – that is what drives blood through the capillary system that exists at different heights in that water column)
  • heart has around 10 mmHg, which is just enough pressure to get it back into heart
197
Q

What do changes in body position do?

A

can alter blood pressure and flow – largely due to changes relative to gravity

198
Q

What happens to blood when you stand up?

A

pooling of blood in lower body

  • ↓ venous return, ↓ SV, ↓ MAP
199
Q

What does the baroreceptor reflex do?

A

brings MAP back to normal

  • ↑ HR and ↑ SV to raise MAP
  • happens within seconds of standing up
200
Q

What is orthostatic hypotension?

A

low blood pressure upon standing when (baroreceptor) reflex is too slow

201
Q

How do vessels respond when giraffes have their head up vs. when they have their head down?

A

vasoconstriction of vessels in lower body when head up

  • prevents pooling in body
  • like compression socks

vasodilation of vessels in lower body when head down

  • compensates for larger pressure changes
202
Q

Why do giraffes have much more dynamic control of vasoconstriction/vasodilation?

A

because pressure difference is large

203
Q

When lying down, what happens to blood pressure when a giraffe lifts their head off the ground? Why?

A

aortic blood pressure increases in order to pump and make sure blood gets to brain

  • fairly rapid response in blood pressure to make sure blood gets to brain, otherwise will lose consciousness within seconds
204
Q

How do giraffes generate enough pressure to get blood flow to their head?

A
  • heart must generate sufficient pressure to overcome hydrostatic pressure
  • thick-walled heart with low stroke volume and fast heartbeat generates super high MAP to overcome gravity
205
Q

What do giraffes have on their feet to withstand pressure?

A
  • giraffe arteries are usually muscular
  • tight skin/endothelium on legs (compression stocking) prevents water loss and pooling – otherwise loose leaky vessels would cause edema
  • venous valves
206
Q

Are muscular pumps more important in humans or giraffes?

A

important in humans (difference between passing out or not if standing still for an hour), but in giraffes it is even more important to take advantage of respiratory pumps

207
Q

Gravitational Effects on Cardiovascular Function in Air and Water

How does pressure change with the height of the water column in air? What does this result in?

A

pressure increases with height of water column

  • pooling at bottom where pressures are high
  • constriction of legs (somewhat equivalent to compression stockings) to prevent pooling, but pressures are the same
  • density of air exerts almost no effect
208
Q

Gravitational Effects on Cardiovascular Function in Air and Water

How does pressure change with the height of the water column in water? What does this result in?

A

blood (and body tissue) and water have similar density, and hydrostatic effects outside the animal cancel out gravitational effects

  • lower in column still means higher pressure – but because water outside column is exerting same pressure inside column, they cancel each other out
  • like having compression stockings – no pooling associated with being vertical in water because density of water is similar to density of blood and body fluids
  • does not change much for an animal at depth because we are looking at relative pressure difference between tail and head – total pressure may be higher, but relative pressure is the same
209
Q

Were sauropods likely aquatic?

A

yes

  • removes gravitational effects for lower region of body
  • heads were more likely oriented horizontally, more or less level with the heart most of the time

+ BIOL 364 (5 decks)

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