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Function of the Body: Section 1 > Section 1 > Flashcards

Section 1 Flashcards

1
Q

Is the autonomic nervous system CNS or PNS?

A

Has selected portions of both CNS and PNS

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2
Q

What are the two primary parts of the autonomic nervous system (visceral)?

A

Visceral sensory - originates FROM sensors in organs
Visceral motor - Modulates organ activity
- targets are the internal organs, mostly the smooth muscle

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3
Q

Function of the visceral nervous system?

A
  • Maintain homeostasis by innervating the smooth and cardiac muscle and the glands
  • Will make adjustments to ensure optimal support for the body
  • Takes part in the fight-or-fligh response
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4
Q

Types of internal and external stimuli for the ANS

A

Internal - pain, hunger, temp- nausea, thirst

External - light, external threat

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5
Q

Quickly review the autonomic receptors (Don’t need to know for exam)

A

Damn it

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6
Q

Primary difference between muscarinic and nicotinic receptors?

A

Speed! Muscarinic are much slower b/c they use G proteins

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7
Q

Do the chart with the differences between ANS and CNS synapses

A

Damn it

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8
Q

What is the primary difference between the innervation of the visceral and vascular smooth muscle innervation?

A

(Lect 2, slide 9)
The visceral has layers where the axons will go in and out of
Vascular, the axons will only stay on the surface. This will allow for the smooth muscle cells within the lumen to counteract the outside

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9
Q

Draw the Adrenergic synthesis pathway

A

Damn it

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10
Q

Draw the ACh synthesis cycle

A

Damn it

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11
Q

What is the precursor for norepinephrine?

A

Dopa

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12
Q

What are the different fates of NE when it is released from the cell?

A
  • Interact with adrenergic receptors (alpha 1 in smooth muscle)
  • Rapid re-uptake and then degradation
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13
Q

Where is the degradation enzymes for Neurepinephrine?

A

cytosol, mitochondria and in the circulation

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14
Q

What is the precursor for Ach?

A

choline (found in egg yolks, liver, soy beans)

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15
Q

How is ACh inactived?

A

use hydrolysis via acetyl cholinesterase

- Occurs very rapidly, and can be very short lived

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16
Q

How does sarin gas effect people and what is the antidote?

A

Inhibits AChE and prevents ACh degradation, causing death in minutes by overstimulation (convulsions, paralysis, respiratory failure)
- Antidote is treatement with diazepam, atropine to block muscarinic AChRs, and pralidoxime to recover AChE fxn

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17
Q

Does ACh linger?

A

No , very short lived

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18
Q

What happens to choline after ACh is degraded?

A

it can be re-uptaken into the presynapticl terminal for reuse

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19
Q

Divisions of the ANS

A
  1. Sympathetic - thoracic and lumbar segments
  2. Parasympathetic - preganglionic fibers leaving the brain and sacral segments
  3. Enteric - controlled by CNS but also works independently
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20
Q

General overview of the two-neuron pathway

A
  • Have a preganglionic neuron, soma located in the spinal cord that synapses onto a postganglionic neuron located in an autonomic ganglion;
  • the postganglionic neuron synapses witht he target organ
  • In general, these will communicated via nicotinic receptors as they must be very fast
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21
Q

Relationship between sympathetic and parasympathetic parts of the autonomic nervous system

A
  • complementary and coordinated, typically produce opposing effects
  • in general, target organs present dual innervation from each
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22
Q

Describe the preganglionic neurons

A

Secrete ACh, which acts on postganglionic nicotinic receptors (ionotropic, fast-acting)

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23
Q

How are the adrenal glands an exception in the ANS?

A
  • There is no post-ganglionic neuron, the synapse is directly on the gland.
  • Direct cholinergic activation causes body-wide release of epinephrine and NE secretion directly into the blood stream
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24
Q

What does the adrenal secrete?

A

80% of Epinephrine and 20% of NE into the circulation

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25
Q

How are the sweat glands an exception to the normal ANS?

A

innervated by the sympathetic branch but are activated via ACh binding to muscarinic metabotropic receptors

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26
Q

Chart of differences between sympathetic and parasympathetic

A

Do it

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27
Q

Visceral afferent fibers

A

Sensory afferents travel from the periphery to the SC and the CNS

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28
Q

How are pain receptors in the viscera activated?

A

distension, ischemia, or obstruction.
- Signals travel through sympathetic nerves to the SC, activate interneurons that trigger reflex arcs, and also activate projection neurons that trigger pain signals to the brain

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29
Q

Referred pain

A

Pain from the viscera that is perceived as somatic pain due to convergence of fibers

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30
Q

Reflexes

A

afferents that travel in the parasympathetic nerves

- use glutamate as the NT and treated with neuromodulators

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31
Q

How are baroreceptors controlled? (Ie. what kind of channels)

A

Uses mechanically sensitive ion channels

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32
Q

What nerve do the baroreceptors use to regulate and where does it synapse?

A

Use the glossopharyngeal nerve that synapses in the medulla

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33
Q

What are the key autonomic centers in the brain?

A
  • reticular formation (brainstem)
  • medulla
  • pons
  • hypothalamus
  • amygdala
  • cortex
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34
Q

Single vs multi-unit muscle?

A

Cardiac is single and skeletal is multi unit.

  • single unit behaves like one single unit
  • multi unit has multiple parts. Can be controlled by nerves
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35
Q

Four major muscle characteristics?

A
  1. Contractility - contractin
  2. Excitability - responds to stimulation by nerves or hormones
  3. Extensibility - muscles can be stretched to normal resting length and beyond
  4. Elasticity - If stretched, can recoil
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36
Q

Functions of muscle

A

Motion
Posture
Heat production

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37
Q

What ECM holds the muscle myofibrils?

A

Endomysium made up of collagen

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38
Q

Label the skeletal muscle

A

Label

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39
Q

Nerve to muscle fiber ratio?

A

One nerve ending for Each muscle fiber

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40
Q

Name the connective tissue sheaths of the muscle and what they surround.

A
  • Endomysium: surrounds individual fibers, contains capillaries
  • Perimysium: surrounds each fascicle, contains blood vessels and nerve
  • Epimysium - surrounds entire muscle
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41
Q

What makes up the tendon?

A

Epimysium, perimysium, and endomysium all come together at the ends of muscles to form tendons

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42
Q

Fascicle

A

A group of muscle fibers

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43
Q

Myofiber

A

muscle fiber = muscle cell

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44
Q

Myofilaments

A

Myosin and actin

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45
Q

Myofibril

A

Composed of many repeating sarcomeres

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46
Q

What is the basic contractile unit?

A

Sarcomeres

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47
Q

Draw the parts of the sarcomere

A

Draw

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48
Q

What parts of the sarcomere stays the same/changes when it is stretched?

A 
Light band (actin) Stretches
Dark band ( Myosin) Stays the same
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49
Q

Thick filament

A
  • Myosin
  • Polymer has ~ 200 myosin molecules
  • Myosin binds actin and has ATPase ACTIVTY (uses globular head)
  • Each pair of heads is oriented 120 deg from the next pair so myosin thick interacts with thin filament in 3D
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50
Q

Thin Filament

A
  • Has Actin, Troponin, and Tropomyosin
  • F-actin is a double stranded Helix composed of many G-actin monomers
  • Thin filament has several interacting proteins: F-actin, Tropomyosin, Troponin-T , -I, -C
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51
Q

Free concentration of Ca in the blood? Cell?

A

~ 1mM

~ 10 nM, So gradient is HUGE

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52
Q

What does troponin-C bind?

A

Binds Calcium

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53
Q

How many tropomyosin and troponin complex per actin?

A

~ 1 per 7 actin monomers

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54
Q

What does troponin-I bind?

A

Actin

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55
Q

Explain the overall process of myosin binding on actin

A

Each G- actin has a binding site for myosin. At rest the binding site is blocked by the troponin-tropomyosin complex. When activated by Ca2+ the troponin-tropomyosin move into the actin groove, myosin binding site on actin is exposed

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56
Q

Which protein makes up most of myofibril?

A

Actin and myosin > 70%

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57
Q

Sarcolemma

A

The plasma membrane of muscle fibers

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58
Q

T-tubule

A

Invaginations of sarcolemma into the muscle fiber, conduct muscle action potential, and are closely apposed to sarcoplasmic reticulum.

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59
Q

What is the voltage sensor on the t-tubule?

A

Dihydropyridine receptor

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60
Q

Sarcoplasmic reticulum

A

A special type of smooth ER of muscle, store a high concentration of Ca. Ryanodine Receptor is the CA releasing channel

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61
Q

Muscle Triad

A

Association of one T-tubule with two adjacent lateral sacs of SR

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62
Q

SERCA

A

sarcoplasmic and endoplasmic reticulum Ca ATPase - a Ca ATPase pump in the SR membrane. Pumps Ca from cytoplasm into SR lumen to restore Ca gradient

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63
Q

Explain the Neuromuscular Junction

A

communication between the muscle and nervous system. The impulse arrives at the end bulb, chemical transmitter is released and diffuses acrosses the neuromuscular cleft. This signals receptor which opens ion channels, Na+ diffuses in and the membrane potential becomes less negative. If threshold is met an action potential occurs and travels along the sarcolema causing contraction

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64
Q

Which receptor takes information from the nerve to start the contraction?

A

Acetylcholine receptor on the postjunctional membrane. It is a nicotinic and opens as a cationic channel (mainly Na+)

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65
Q

Does the sodium that enters the muscle cell when activated with ACh cause the upstroke and potential?

A

No, the Na only activates the voltage gated sodium channels

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66
Q

What are the steps in the EC coupling?

A
  1. Action potential travels into T-tubule
  2. Depolarization activates DHPR
  3. DHPR conformational change activates RyR
  4. Ca release from SR
  5. Ca initiates muscle contraction
  6. SERCA pumps Ca back into SR lumen (muscle relaxes)
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67
Q

Why can a skeletal muscle contract even if it’s isolated and placed into a bath with no Ca?

A

Thought the DHPR voltage gated Ca channel is a Ca channel, it does not allow Ca out. Thus, the Ca within the SR will remain inside the cell allowing for contraction.

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68
Q

What are the relative times of the change in Ca concentration compared to the twitch of a muscle?

A

The change in Ca concentration will occur very quickly compared to the actual contraction. See lecture 3 slide 26

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69
Q

Steric hindrance effect on troponin/tropomyosin, etc.

A
  1. Calcium binds troponinC
  2. Conformational change so troponin I has LOW actin affinity
  3. Tropomyosin and troponins move into actin groove
  4. Myosin binding site on actin is exposed
  5. Myosin binds actin–> Crossbridge cycle
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70
Q

Draw the cross bridge cycle

A

Damn it

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71
Q

Since Action potentials are musch faster than a muscle twitch, what does that allow one to do?

A

If you do many action potentials in a row at higher frequencies you will get a summation of twitch force until eventually you reach tetanus

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72
Q

Ways to modulate force of muscle

A
  1. Can increase frequency of action potentials
  2. Recruitment of more motor units
  3. Muscle fiber thickness (ie. more sarcomeres in parallel)
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73
Q

Explain the effect of length of fibers and contraction strength

A

If sarcomere is too short - steric hindrance

if sarcomer is too long - not enough crossbridges overlap with actin so there is less force

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74
Q

Draw a rough force-velocity relationship

A

Damn it

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75
Q

What determines how much muscle force you can have?

A

The number of myosin and actin interactions available.

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76
Q

What determines velocity of contraction

A

the speed at which cross bridges cycle. Which varies by muscle type

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77
Q

Concentric contraction

A

Muscle actively shortening

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78
Q

Eccentric Contraction

A

Muscle actively lengthening
Causes muscle injury, soreness, and increases muscle strength.
Idea of a shock absorber

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79
Q

Isometric contraction

A

Muscle actively held at a fixed length

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80
Q

Passive stretch

A

Muscle passively lengthening likely resulted from a giant protein called Titin within muscle fiber

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81
Q

Isotonic Contraction

A

The tension on the muscle stays the same

Can be either concentric or eccentric

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82
Q

How is ATP used in contracting muscle?

A

Actomyosin ATPase (ie. crossbridge) is ~ 50-70% of all ATP consumed
- Other ATP-consuming processes: SERCA - 20-30%
Na/K ATPase

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83
Q

Sources of ATP

A
  1. Creatine phosphate
  2. Oxidative phosphorylation (mitochondria)
  3. Glycolysis
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84
Q

What catalyzes the reaction of creatine-P to ATP? Is this a fast or slow reaction?

A

Use creatine kinase

This is a rapid release of ATP

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85
Q

What is the first energy storage in muscle?

A

Creatine is the first, but is depleted in just a few seconds

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86
Q

Oxidative phosphorylation

A
  • Occurs in mitochondria
  • Aerobic process
  • Slow synthesis (but efficient) 30 ATP per glucose
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87
Q

What is the oxygen binding molecule in muscles?

A

Myoglobin, a red color. This tissue has alot of mitochondria and alot of blood vessels

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88
Q

Glycolysis

A

anaerobic process that is FAST and INefficient at creating ATP.

  • Produces lactate
  • 6 ATP per glucose
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89
Q

Different forms of muscle fatigue

A
  • lactate is generated in glycolysis
  • decreased pH - inhibits enzymes
  • depletion of energy reserves
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90
Q

Myasthenia gravis

A

Not normal in healthy people

Neuromuscluar fatigue that causes muscle fatigue

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91
Q

Muscle type chart

A

Do it

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92
Q

Does the dihydropiridine receptor allow calcium out?

A

NOT in skeletal muscle

In cardiac muscle, it does. The amount of calcium flux actually controls the strength of the contraction.

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93
Q

How is the strength of contraction in the heart differ than in skeletal muscle?

A

Skeletal muscle uses recruitment or increase AP frequency

Cardiac muscle uses differential flux of Ca in and out of DHPR. This is modulated by phosphorylation by PKA.

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94
Q

Why does smooth muscle appear smooth?

A

The actin and myosin are more randomly distributed. Not in organized patterns like in striated muscle. Further they have no t-tubules. Uses dense bodies

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95
Q

Draw the mechanism of smooth muscle contraction

A

Damn it

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96
Q

What is differences between smooth muscle and striated muscle contraction?

A

Smooth uses MLCK to phosphorylate the myosin. There is no troponin, so the actin is always available when the myosin is active

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97
Q

Is basal tone the same in all smooth muscle?

A

No, can be a number of different things:

  • sphincters - normally contracted
  • blood vessels : normally partially contracted with some changes
  • Stomach/Intestines : Phasically active
  • Esophagus, bladder: Normally relaxed and then is stimulated to contract
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98
Q

Describe EC coupling in smooth muscle

A

Can occur through a number of ways:

  1. An intrinsic nerve that effects multiple cells in a multi unit manner
  2. Diffusion of neurotransmitters through the capillaries
  3. Single units where the nerve will effect and then signal is propagated
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99
Q

Smooth Muscle Cell Activation pathways that require and DON”T require membrane depolarization

A

DO NOT: IP3, cAMP, cGMP

DO: Voltage gated Ca, Ligan bound Ca, Ca entry effect Ca-CaM and MLCK

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100
Q

Do chart of differences between different types of muscles

A

Damn it

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101
Q

Agonists and response of smooth muscle activy

A

Damn it

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102
Q

How much blood does a ventricle hold? How much is ejection volumen?

A

150 ml

80 ml

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103
Q

Does the AV node speed up or slow down conduction?

A

Slows down, it gives the atria a chance to actually do their job.

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104
Q

Purkinje fibers

A

Activate all of the ventricular cells (ie. endocardium). Allow coordinated ejection of blood vs. sloshing around

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105
Q

Heat block

A

Failure of conduction somewhere in the pathway, easily seen in the EKG

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106
Q

Papillary muscles

A

Ensures valves leaflets don’t blow backwards. Found by having pappillary muscles die, chordae tendinae dont work, leaflets go backwards

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107
Q

Is the EKG the action potential?

A

No, it is caused by the AP. It is actually the propagation of the AP through the heart.

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108
Q

Draw the EKG components

A

Damn it

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109
Q

Why don’t see electrical event of Atrial repolarization?

A

Gets lost in the QRS wave

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110
Q

What is the QR interval?

A

Time it takes from the atria activation to the ventricle activation (beginning of the P to beginning of the Vent depol)

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111
Q

What causes the resting membrane potential of cardiac cells?

A

The relative permeability of ions (Na, K, Cl, etc)

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112
Q

What causes the gradients of ions for resting membrane potentials?

A

Na-K pump

  • works in two directions at the same time
  • Uses alot of ATP
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113
Q

Na-K pump

A
  • maintains Na/K gradients
  • elctrogenic (net outward current)
  • needs ATP
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114
Q

Digitalis

A

A specific inhibitor of Na-K pump
Causes the heart to beat HARDER
- Through indirect effects

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115
Q

Na-Ca exchanger

A
  • exchanges 3 Na for 1 Ca (electrogenic net inward current)
  • Forward direction: extrudes intracellular Ca to maintain low intracellular Ca
  • Driven by the Na gradient across teh membrane, therfore indirectly affected by alterations in Na/K pump
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116
Q

Drugs against the Na-Ca exchanger. Why? danger?

A
  • Can be used to ensure Ca is reserved in the SR

- If too much is conserved, it can cause too large of a contraction which will result in arrythmias

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117
Q

Inward rectification

A

If the K outside of the cell is reduced, Kir channels will decrease the permeability of K. Thus, less K leaking out means that the resting membrane potential will be less negative than it technically should be in this. This will ensure that the cell can conserve K.

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118
Q

Why is it important for the potassium channels to turn off when the heart depolarizes?

A

So it stops fighting the upstroke of the AP

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119
Q

Hyperkalemia

A

Abnormally high (> 5meq/L) extracellular K

  • increases the membrane K permeability
  • decreases K concentration gradient across the membrane
  • effect is a more positive membrane potential, generally fatal
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120
Q

Hypokalemia

A

Abnormally low (

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121
Q

How is the time scale of a cardiac AP compared to a neuronal AP?

A

Cardiac is much longer than the neuronal

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122
Q

Do the Ionic mechanism of Cardiac AP for: Ventricle, SA node, and Atrium

A

Draw this 100 times and explain the phases!!!!

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123
Q

When looking at the membrane potential of the ventricular contraction, why is it “best of both worlds?”

A

The Na channels cause a very fast action potential and the Ca is slow. Thus Calcium causes for the long plateau, which allows for contraction to occur

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124
Q

Do Nerve cells use Ca in their action potentials?

A

No, they don’t need time to contract so they don’t need to stay depolarized for so long

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125
Q

What nernst potential does the repolarization go to?

A

K Nernst potential using the delayed rectifier K channels

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126
Q

What is the clock for the rhythm of the heart?

A

It is the potential differences in the SA node. The SA node has no “resting potential” it is constantly drifting, once it drifts high enough it will fire the AP. THIS is what allows the heart to beat automatically

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127
Q

What does tetrodotoxin do?

A

Blocks the Na channel. So converts that fast response into a slow response. The slow Ca channel now is in charge of the upstroke

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128
Q

Does TTX effect phase 0?

A

Yes, it effects the FAST upstroke, so with TTX there is still an upstroke; however, it is done by the slow Ca channels

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129
Q

Intercalated discs

A

Specialized region of intercellular connections betwen cardiac cells. Has 3 types within the disc:

  1. Fascia adherens
  2. Macula adherens
  3. Gap Junctions
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130
Q

Fascia adherens

A

anchoring sites for actin that connect to the closest sarcomere

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131
Q

Macula adherens

A

Holds cells together during contraction by binding intermediate filaments, joingin the cells together. These junctions are called desmosomes

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132
Q

Gap Junctions

A
  • low resistance connections that allow current to conduct between cardiac cells
  • intracellular connections through connexon channels
  • primary determinant of resistance
  • Sensitive to intracellular Ca and H ions
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133
Q

Healing over

A

an increase in internal resistance that results from a decrease in the number of open gap junctions

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134
Q

What causes healing over?

A

caused by an increase in intracellular Ca and/or H ions

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135
Q

Structure and function relationship for different parts of the cell

A

Do the chart

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136
Q

What effects the rate of the cardiac action potential?

A
  1. Space constant (Rm/Ri)^1/2
  2. rate of rise AND amplitude of the AP
    - slow vs fast response AP
    - premature responses initiated during relative refractory period
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137
Q

How does the resting membrane potential and Na channel availability relate?

A

If resting potential is MORE positive then the number of fast Na channels available for activation will DECREASE. THus conduction will slow down

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138
Q

What types of conditions can influence the AP upstroke as a result of changes in the resting membrane potential?

A
  1. hyperkalemia (more positive RMP)
  2. Premature excitation during relative refractory period
  3. ischemia or myocardial injury
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139
Q

What occurs with cardiac cells in hyperkalemic state?

A

The fast acting Na channels will slowly stop working as well and the conduction will be slow and look more like a node

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140
Q

P-R interval

A

Part of the EKG shows the health of the AV node. Shows conduction time from atria to ventricular muscle

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141
Q

QRS interval

A

Intra ventricular conduction time

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142
Q

AV node conduction

A
  • normally, conduction delay permits optimal ventricular filling
  • action potential is slow repsonse due to slow inward Ca current
  • Relatively long refractory periods
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143
Q

How does the AV node protect the ventricles from atrial flutter or A fib?

A

Since there is a long delay at the AV node it can generally filter that out

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144
Q

HOw is AV node conduction time determined?

A

PR interval of the EKG

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145
Q

Different degrees of heart block

A

1st - abnormal prolongation in PR interval greater than 0.2 sec
2nd - some atrial impulses fail to activate the ventricles (Wenckebach (AV) and Mobitz (His-purkinje))
3rd - Complete disconnect between P-R interval and the QRS complex

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146
Q

DIfferen EKG abnormalities with ventricular conduction

A
  1. slurred QRS complex indicates slowed intra-ventricular conduction. Causes could he hyperkalemia, ischemia, ventricular tachycardia
  2. Notched QRS complex indicates asynchronous electrical activation of left and right ventricles. Causes: lef and/or right bundle branch blocks
  3. Ventricular conduction during different types of tachycardia
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147
Q

Compare the EKG of someone in A fib compared to V-fib

A

A fib will have alot fo squiggly line before APs, can have an irregularly irregular heartbeat; however, it is compatible with life.
V-fib is lines all over the place and is not compatible with life. Basically have about 2 mins to shock a patient back.

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148
Q

Draw effect of the Vagus Nerve

A

Damn it

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149
Q

How does norepinephrine affect the heart?

A
  • Sympathetic
  • Affects ALL areas of the hear
  • Acts primarily via B-1 adrenergic receptors to increase cAMP
  • INcreases slow inward Ca current
    • increases SA node rate (decrease r-r interval)
  • INcreases AV node conduction (decrease the P-R interval)
  • Increases atrial and ventricular muscle contraction: positive ionotropic response
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150
Q

How is the heart rate effected in a heart transplant patient?

A

Since the vagus nerve will be effected the heart will beat at a fairly high resting HR.

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151
Q

How does the parasympathetic ANS effect the ventricular muscle function?

A

There is NO direct effect on the basal ventricular muscles function.
- However, if the ventricals are first pre-stimulated by beta-adrenergic receptor simulation via sympathetic nervous system then ACh can exert a large inhibition by inhibiting sympathetic stimulation mediated by the production of cAMP

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152
Q

Vagus nerve effect on the heart

A
  • Vagus nerve is parasympathetic and releases ACh
  • Acts via muscarinic receptors
  • Increases K permeability via G-protein; thus, ACh decreases slow inward Ca current indirectly via inhibition of cAMP synthesis
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153
Q

How does the vagus nerve effect the atrial muscles?

A
  • Inhibition of atrial muscle: negative ionotropic effect
  • Inhibition of SA node: lengthens PP interval and RR interval
  • Inhibtion of AV node: lengthens PR interval
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154
Q

Fast vs Slow Response Refractory Periods

A

Fast - voltage-dependent refractoriness. As soon as it’s repolarized it’s ready to go again
slow - Primarily time-dependent refractoriness, even after repolarization, it’s still refractory

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155
Q

Premature beats

A

Usually benign, but if one arrives really early, some of the Na channels aren’t recovered yet… leads to a slow upstroke, abnormal conduction. This can lead to reentry of excitation.

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156
Q

R on T

A

A premature beat (R wave) that occurs during the relative refractory period (T wave) of the previous beat.

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157
Q

Commotio cordis

A

Usually occurs in young men (~15) when they get struck in the chest. Can cause a mechanically stimulated AP which can send into an arrhythmia

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158
Q

Slow reponse refractory periods

A

These Ca channels are more dependent on time than on voltage, thus they last longer than the AV node action potetniatl duration. This mechanism is responsible for the fact that conduction through the AV node slows when stimulated at higher rates (short cycle lengths).
- This also prevents rapid ventricular activation during atrial tachy-dysrhythmias such as atrial fibrillation or flutter

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159
Q

How does a stress test uncover arrhythmias?

A

The Stress test will cause the heart to beat faster (ie. shortening the PR interval) This will give a shorter refractory period, allowing visualization of the arythmia

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160
Q

Effects of excitation at various times after a slow response AP

A

Early impulses are abnormally small b/c there aren’t enough Ca channels available to support a normal AP

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161
Q

Why does Atrial fibrillation lead to clotting?

A

Blood can be stagnant in the appendages of the atria. IF you cardiovert you can send the clot into the coronary arteries (heart attack) or up brain or lungs.
- Treat with anticoagulants, agents that lengthen the refractory period, ablation oft he site of arrhythmogenesis

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162
Q

Does systole or diastole change whne trying to speed up or slow down the heart rate?

A

Systole stays relatively the same. Diastole will change to make HR faster or slower

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163
Q

What part of the EKG makes up the Q-T interval?

A

Action potential duration

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164
Q

Prolonged Q-T syndrome

A

an abnormal prolongation of the Q-T interval

  • Acquired through bradycardia, hyopkalemia, drugs
  • OR congenital - due to genetic lesions in Na and/or K channels
165
Q

Torsades de pointes

A

polymorphic ventricular tachycardia

- results from conditions in which the Q-T interval is abnormally prolonged posslby from early after depolarizations

166
Q

What is the primary pacemaker oft he heart?

A

SA node, has the fastest inherent beating rate

167
Q

What is the hierarchy of pacemakers in the heart?

A

SA node –> latent atrial pacemekaer –> AV nodal/His bundle –> bundle branches –> purkinje fibers

168
Q

What mechanisms underlie the SA node pacemaker activity?

A
  • T-type Ca current
  • hyperpolarization-activated inward current (If)
  • deactivation of K current (Ik)
  • Inward Na/Ca exchange current activated by intracellular SR Ca release
169
Q

Funny current

A

If, the pacemaker channel

  • all other channels are activated by depolarizaiton but thisone is activated by hyperpolariztion. It is found in all pacemaker tissues (including the gut)
  • when the cell repolarizes, it turns on this channel, leaks some Na in, causing some of the depolarization
170
Q

Purkinje fiber pacemaker activity

A

Due to the If current and deactivation of K current

171
Q

Do the Ionic current mechanisms of the SA node pacemaker image

A

Do

172
Q

Mechanisms responsible for changes in heart rate

A
  1. change in slope of diastolic depolarization
  2. change in max diastolic potential
  3. change in threshold
  4. Pacemaker shifts - changes in pacemaker site can cause abrupt changes in heart rate b/c of the hierarchy of pacemaker activites (patholigcal)
173
Q

What happens if a pacemaker is stimulated at a frequency higher than the intrinsic one?

A

It will stop. working as a pacemaker and even if the stimulations stop, it won’t recover right away.

174
Q

Can you take a person off of a pacemaker?

A

No, must wean them off to allow the ectopic pacemaker to pick up

175
Q

Vagal nerve stimulation on heart

A
  • inhibits pacemakers withint SA node, atria and AV nodal regions
  • increases K permeability, which will hyperpolarize the cell making it harder to have an AP
  • Inhibits cAMP-dependent slow inward L-type Ca current and If current
  • vagal nerve could be used instead of mechanical pacemakers as therapeutic
176
Q

Sinus arrhythmia

A

Normal variability in pacemaker cycle caused by respiratory changes in parasympathetic (vagal) nerve activity to the SA node

  • inspire causes decrease in cycle length (increase in heart rate) by inhbition of parasym nerve activty. Stretch receptors in the lung feed back and decrease HR
  • Expiration is opposite
177
Q

What causes dysrhthmias?

A

Alteration in impulse formation, impulse conduction, or both.

  • Automaticity
  • Re-entry ecitation
  • triggered activity
178
Q

Automaticity

A

Alterations in pacemaker rate that are mediated through changes in the pacemaker mechanisms that normally exist in pacemaker cells

  • tachycardia - > 100bpm
  • bradycardia -
179
Q

What causes Tachy-dysrhthmias?

A
  1. Norepinephrine (sympathetic nervous activity)
  2. Stimulants (amphetamines)
  3. Stretching (ventricular aneurysm)
  4. Electrolytes (hypokalemia)
  5. Sick sinus syndrome, fever, hyperthyroidism
180
Q

What are some EKG manifestations of altered automaticity?

A
  1. Sinus tachycardia
  2. premature atrial contraction
  3. premature ventricular contraction
  4. atrial or ventricular tachycardia
  5. supraventricular tachycardia
181
Q

Causes of brady-dysrhythmias?

A
  1. Drugs - anti-arrhthmics, Beta-blockers, Ca antagonists, digitalis, barbiturates
  2. Ischemia or infarct
  3. Sick sinus syndrome
  4. aging - fibrosis
182
Q

EKG manifestations of Bradycardia

A
  1. Sinus bradycardia

2. atrial or ventricular premature beats

183
Q

Re-Entry of Excitation

A

The idea where the geometry is such that one conduction will loop around and restimulate part of the heart that has already contracted

184
Q

What are the requirements for re-entry of excitation?

A
  1. geometry for a conduction loop
  2. slow or delayed conduction
  3. unidirectional conduction block
185
Q

Explain why a slow conduction is a precursor for re-entry excitation?

A

If the signal is really fast, then when it gets to tissues that has already contracted it is still in refractory period.

186
Q

Possible causes of re-entry excitation

A
  1. ischemia
  2. infarction
  3. congenital bypass tracts (wolf-parkinsons-white)
187
Q

EKG manifestations of re-entry excitation

A
  1. premature atrial or ventricular beats
  2. atrial or ventricular tachycardia
  3. supraventricular tachycardia
  4. atrial flutter
  5. atrial or ventricular fibrillation
188
Q

What is a basic way to increase cardiac muscle contraction?

A

Have more Ca inside of the cell

189
Q

What causes a delayed afterdepolarization?

A
  • Abnormally elevated intracellular Ca

- Documented with dysrhythmias from digitalis toxicity

190
Q

Causes of Delayed Afterdepolarization?

A
  1. Digitalis toxicity
  2. Elevated catecholamines
  3. Rapid Heart Rate
  4. All in combination
191
Q

EKG manifestionas of Delayed Afterdepolarization

A
  1. Premature Atrial or ventricular contraciton

2. Atrial or ventricular tachycardia

192
Q

Mechanism of triggered activity

A
  • elevated intracellular Ca is taken up by SR
  • When overloaded with Ca, an AP triggers the release of Ca AFTER the AP
  • This causes inward current of Na from the Na/Ca exchanger
  • if large enough to bring the membrane to threshold the AP is generated
193
Q

Early After-depolarizations

A

related to prolongation of action potential duration

194
Q

Causes of early after-depolarization

A
  1. acidosis (as in ischemia)
  2. hypokalemia
  3. quinidine
  4. Slow heart rates
195
Q

EKG manifestations of Early After-depolarization

A
  1. premature atrial or ventricular contractions

2. Atrial or ventricular tachycardia (torsade de pointes)

196
Q

Why does early afterdepolarizations manifest at slower heart rates?

A

Slow HR will lengthen the action potential. Will lead to coupled beats (regularly irregular)
- Can lead to R on T

197
Q

What is the normal P-R interval?

A

0.12 - 0.2 Sec

198
Q

What is the mechanism that noradrenaline and epiephrine use to increase cardiac contractility

A
  1. Binds to B-adrenergic receptors (primarily B1) on the surface membrane
  2. Acts via Gs to activate adenylate cyclase to increase cAMP
  3. cAMP activates cAMP-dependent PKA
  4. PKA phosphorylates
    - Ca channels to increase Ca influx
    - Phospholamban to increase SR Ca uptake (enhances relax)
    - both mechanisms increase Ca induced Ca release (increase strength of contraction
    - Enhances time course of relaxation
199
Q

What happens with phosphorylation of phospholamban?

A

It will no longer inhibit the SERCA pump. Thus, with more SERCA there is more pumping the Ca into the SR. This will allow for quicker relaxation and more Ca to be released when SR is stimulated.

200
Q

Cardiac glycosides

A

Eg. digitalis

- postivie ionotropic agent used in CHF

201
Q

Cardiac glycoside mechanism

A
  1. inhibits the Na-K pump
  2. Lead to increased intracellular [Na] and thereby decreases [Na] gradient
  3. Slows Ca extrusion via Na-Ca exchanger and increases intracellular [Ca]
  4. Increased Ca in cell will elad to increase in SR Ca content so greater SR Ca release and stronger contraction
202
Q

Ca Channel blockers

A

Anti arrhythmic agents

203
Q

Mechanism of Ca channel blockers

A
  1. Blocks Ca influx via Ca channels
  2. decreases in SR ca release and SR Ca content which leads to less contraction in vascular smooth muscle (vasodilator)
  3. Cardia anti-arrhythmic effects due to inhibition of slow inward Ca current which inhibits conduction of the AV node AP
204
Q

Side effects of ca channel blockers

A

Will decrease the cardiac function

205
Q

Force frequency relationship in the heart

A

the beating rate and rhythm of the heart influences cardiac contraction amplitude by altering contractility. Changes in cycle length alter the TIME available for intracellular Ca handling, which alters contractility

206
Q

Positive staircase (treppe)

A

As heart rate increases the strength of the contraction also increases

  • Greater influx of Ca per unit time and less time for Ca efflux via Na/Ca exchange
  • Increased SR Ca content and SR Ca release; larger contraction strength
207
Q

Negative staircase

A

Decrease in heart rate results in decrease in contraction strength

208
Q

Mechanism of negative staircase

A
  1. less Ca influx per unit time and more time for Ca efflux
  2. Less SR Ca content
  3. Thus, smaller Ca induced Ca release; smaller contraction strength
209
Q

Post-extrasystolic potentiation

A

Stronger than normal contraction of the beat following a premature beat

210
Q

mechanism of post-extrasystollic potentiation

A
  1. More time for recovery of Ca
  2. More time for recovery of SR Ca release
  3. MOre time for redistribution of Ca stores into the terminal cisternae of SR
  4. Thus, larger Ca induced Ca release; larger contraction strength
211
Q

Factors that determine cardiac outpu

A
  1. Heart rate
  2. myocardial contractility
  3. Preload
  4. Afterload
212
Q

Preload

A

Load on the muscle before contraction is initiated. The preload stretches the muscle length and therefore generates passive tension on the muscle

213
Q

What dictates the preload

A

Ventricular filling

214
Q

Afterload

A

Load on the muscle after contraction is initiated. Any force that resists muscle shortening

215
Q

Contractility

A

inherent abilit of actin and myosin to form cross-bridges and generate contractile force. it is independent of preload and afterload. Primarily determined by intracellular Ca

216
Q

Is muscle contraction only associated with muscle shortening?

A

No, Isometric and Isotonic

217
Q

Isometric Contraction

A

No change in length.

218
Q

Isotonic Contraction

A

Contraction with shortening and constant force. If a muscle is able to generate enough force to meet the afterload

219
Q

What determines the resting tension curve?

A

The muscle compliance

220
Q

Active tension

A

Amount of isometric tension that is developed by muscle contraction at a partiular muscle length (preload).Slope is determined by contractility

221
Q

Compliance

A

Change in volume in relation to a change in pressure

222
Q

Is skeletal or cardiac muscle more compiant?

A

Skeletal

223
Q

How does an increase in preload cause an increase in tension development?

A
  1. creates more optimal overlap betweeen thin and thick filaments
  2. increaes Ca sensitivity of myofilaments
224
Q

WHAT happens to muscle shortening when you increase or decrease the preload?

A

An increase in preload increases the amount of muscle shortening(Chart on slide 9 lecture 12)

225
Q

What happens with increased afterload?

A

Amount of isotonic tension is greater but the amount of muscle shortening decreases. Think of it as, if the blood pressure goes higher and higher it’s harder for the heart to pump

226
Q

When looking at a Pressure-volume cardiac diagram, what causes the aortic valve to open?

A

When the pressure in the ventricle surpasses the afterload (aka. the pressure in the aorta)

227
Q

Why does ejection of blood from the heart stop?

A

Look at the contractility curve. When the heart is active at normal contraction, at different lengths it has different amount of force. So during ejecting, it will continue to eject until it hits its’ physiological limit.

228
Q

What happens to the contractility curve when you add adrenaline?

A

The curve will go higher, so the potential limit is higher.

229
Q

Contractility/Length/Tension curves

A

Lecture 12 just do everything

230
Q

Keeping everything equal, what does an increase in contractility accomplish?

A

Increases the amount of muscle shortening by allowing the muscle to reach a shorter length

231
Q

Compare contractility and contraction force

A

contractility - is the ability for the muscle to shorten which is directly correlated to the amount of Ca available. Increase also increases velocity of shortening and increases the rate of relaxation

Contraction strength - relies on pre and after load.

232
Q

How does afterload effect the shortening velocity?

A

Larger afterload leads to slower shortening velocity until you reach the maximum isometric force

233
Q

Do Force-velocity graphs (regular, increased preload, increased afterload)

A

Do it

234
Q

What can increase stroke volume?

A
  1. Increase Preload
  2. Decrease Afterload
  3. Increase Contractility
235
Q

What happens to the P-V curve with Heart failure?

A
  1. Systolic heart failure will have decreased ventricular contractility, thus, will have a larger end systolic volume and a smaller ejection fraction.
  2. In diastolic heart failure will have lower end diastolic volume
236
Q

Cardiac output?

A

Stroke volume x Heart Rate

237
Q

What effects the stroke volume?

A
  1. Pressure gradient between atria and ventricles
  2. Time for ventricular filling
  3. Ventricular compliance
  4. Atrial function
238
Q

How does an increase in the end-diastolic pressure effect ventricular filling?

A

decreases

239
Q

Effect of increased heart rate

A

increase contractility

decreases the time for ventricular filling

240
Q

How does the sequence of activation affect the efficiency of ventricular filling?

A

Arrhythmic activity and abnormal sequence of activation will decrease the efficiency

241
Q

Central Venous Pool

A

Corresponds to the volume enclosed by the right atrium and the great veins in the thorax

242
Q

Venous Return

A

Rate a which blood returns to the thorax from the peripheral vascular beds

243
Q

Under normal steady-state how does venous return and cardiac output relate?

A

Should be equal

244
Q

Central venous pressure

A

Is the pressure in the venous system. WIll decrease as cardiac output increases. With 0 cardiac output the mean circulatory pressure should be 7 mmHg

245
Q

How can the central venous pressure predict heart failure?

A

With heart failure, the central venous pressure will increase due to a decrease in cardiac output. Thus, can be used diagnostically

246
Q

Graph the central venous pressure vs. cardiac output

A

Do it

247
Q

What happens when the central venous pressure equals the mean circulatory pressure?

A

There is no pressure gradient for venous reture (thus, no blood flow)

248
Q

How does an increase in cardiac outpu effect venous reture?

A

Will increase the pressure gradient, thus increases the venous return

249
Q

What increases peripheral venous return?

A
  1. Increased sympathetic venoconstriction
  2. Increased blood volume
  3. increased skeletal leg muscle pumping activity
250
Q

What decreases central venous pressure?

A
  1. respiratory pump activity (taking breaths sucks up blood)

2. Cardiac suction (when the blood relaxes there is a natural rebound)

251
Q

How does the venous valves influence the venous return?

A

Will maintain the pressure gradient between peripheral and central venous pools in the face of gravitation forces

252
Q

Draw the factors that influence venous return

A

Draw it

253
Q

What happens to the central venous pressure vs cardiac output when you have hemmorhage or transfusion?

A
  1. Hemmorage - Decreases venous return

2. Transfusion - Increased venous return

254
Q

How does sympathetic nerve activity effect the CVP vs Cardiac outpu chart?

A

Increased venous tone - Increases venous return

Decreased in venous tone - Decreased venous return

255
Q

Effects of Heart Failure

A
  1. Shifts the cardiac function curves down, thus cardiac outpu decreases and CVP increases
  2. Kidnes will increase the blood volume which shifts the vascular function curve upward and to the right (hypervolemia), this increases CVP
    Moderate - elevated CVP improves the preload so that there is little reduction to the cardiac outpu
    Severe 0 hearts contractility is reduced so much that the cardiac output cannot be maintained
    - Increased CVP causes pumonary congestion and pitting edema in the extremities
256
Q

Cardiovascular adjustments to hemorrhage

A
  1. Venoconstriction
  2. Arterial vasoconstriction
  3. Cardiac contractility is increased by increased sympathetic activity (eg. adrenaline)
  4. Low BP results in dialysis of fluid from the tissues, partially restoring lost blood volume
257
Q

Describe flow in regards to Pouiseulille’s law

A

Flow is directly proportional to the pressure gradient and radius raised to the 4th power
- Flow is inversely proportional to the vessel length and blood viscosity

258
Q

Resistence

A

R = 8/pi x (L x viscosity)/ radius ^4

259
Q

Why are the R and L ventricular pressures different if they generate the same cardiac output?

A

B/c they have different resistence

260
Q

Viscosity

A

Internal frictional resistance between adjacent layers of fluid

  • Depends on the shear stress and shear rate
  • = Shear stress/ shear rate (pressure/velocity)
261
Q

What is the shape of blood flow?

A

Have more shearing on the farther out walls, inner most cylinder moves with the highest velocity. Thus, there is a parabolic profile

262
Q

Newtonian vs Non-newtonian fluids

A

newtonian - viscosity remains constant over a range of shear rates
- non newtonian - viscosity changes over a range of shear rate and shear stress (occurs in blood b/c of RBC, WBC, proteins)

263
Q

Normal hematocrit range

A

35-50%

264
Q

How does viscosity change with increased % of hematocrit?

A

Will increased very rapidly

265
Q

Anemia

A

Low hematocrit, relatively low viscosity

266
Q

Polycythmia

A

High hematocrit, relatively high viscosity, increased erythropoietin. Can lead to multiple myeloma

267
Q

Axial streaming

A

Tendency of RBCs to accumulate in axial laminae at high shear rates

268
Q

Plasma skimming

A

occurs due to axial streaming

is the tendency of smaller vessels to contain relatively more plasma and less RBCs

269
Q

If the blood flow slows down in smaller vessels what happens to the viscostiy of blood?

A

It should increase, but it doesn’t in small vessels b/c of axial streaming

270
Q

Relative hematorcrit in smaller vessels compared to larger vessels

A

Hematocrit is lower in smaller vessels compared to larger vessels

271
Q

Spherocytosis

A

RBCs are spherical and can’t change shape to enter capillaries resulting in anemia

272
Q

Laminar flow

A

Fluid moves in parallel concentric layers within a tube, silent

273
Q

Turbulent flow

A

Disorderly pattern of fluid movement, non-laminar

- Murmurs, damage to endothelial lining, thrombi, korotkoff sounds

274
Q

Reynold’s number

A

dimensionless number indiciating propensity for turbulent blood flow. The higher the reynold’s number (>3000), the greater the chance for turbulent blood flow to develop

  • Determinants - tube diameter (D), velocity (v), density (p), viscosity (n)
  • = pDv/n
275
Q

What causes the noises in turbulent flow

A

Really is the velocity

276
Q

Compare velocity of blood and cross-sectional area

A

Velocity of flow varies inversely with cross-sectional area

277
Q

Do the small vessels in the normal circulation have high velocity flow?

A

No, b/c they have so many smaller branches.

278
Q

Wall tension

A

Tension that holds the vessel open. = Pressure x Radius/Wall thickness

279
Q

Do capillaries withstand alot of pressure?

A

Yes, small radius = low wall tension, thus can withstand a large trans-mural pressure

280
Q

How does the thickness of areteriol supply effect the tension

A

Large wall thickness/lumen diamter ratio = low wall tension

281
Q

Aneurysm effect on wall tension

A

Large radius fromt he aneurysm leads to high wall tension, cannot withstand trans-mural pressures and therefore will rupture

282
Q

Dilated Hearts and tension

A

Large radius = high wall tension; more systolic work to overcome higher wall tnsion. Afterload opposes shortening. Overall, this is going to lead to higher oxygen consumption

283
Q

What percentage of blood do the following things use?

  1. Cerebral
  2. Coronary
  3. Renal
  4. GI
  5. Skeletal muscle
  6. Sking
A
  1. 15%
  2. 5%
  3. 25%
  4. 25%
  5. 25%
  6. 5%
284
Q

What is the signal for needing blood

A

When one part of the body is working overtime it will create alot of metabolites (CO2, Use of ATP, etc). Local control will cause rest of body to do sympathetic

285
Q

Where is most of the blood volume in the body/

A

Most is in the veins

286
Q

Where is resistance highest?

A

Largest at the arterioles. Thus, largest drop in pressure is across the resistance vessels

287
Q

Why is the drop in pressure across the capillaries so small?

A

Capillaries have the largest TOTAL cross-sectional area. Therefore, the drop in pressure is small

288
Q

How does the mean arterial pressure chance as you move away from the heart?

A

Continuously decline throughout the circulatory system

289
Q

Where is the greatest decrease in arterial pressure?

A

Arterioles

290
Q

What determines the mean arterial pressure

A

Mostly the diastolic pressure

291
Q

How does the systolic and diastolic pressure change as you move away fromt he heart

A

Systolic increases and diastolic decreases

- Due to reflection at branch points, vascular taperin, decrease in arterial compliance

292
Q

What gives arteries the compliance?

A

Internal Elastic Lamina

293
Q

Tunica Intima, Media, Adventitia

A

Intima - Subendothelial connective tissue, internal elastic lamina
Media - smooth muscle cells and external elastic lamina
Adventitia - Mostly connective tissue with some smooth muscle cells; vasa vasorum, innervation nerves

294
Q

Compare artery and veins

A

Artery has elastic lamina, veins don’t
artery has more smooth muscle than veins
artery has LESS connective tissue (adventitia) than veins

295
Q

Most to least compliance

A

Elastic lamina
Smooth Muscle
Collagen

296
Q

How do the compliance characteristics of these tissues affect arterial pressure?

A

Less compliance will give more pressure

297
Q

Continuous Capillary

A 
Continous endothelial cells
no holes in the capillary wall
tight junction between cells
Continuous basal lamina
Muscle and connective tissues
298
Q

Fenestrated capillary

A

Continuous endothelial cells with hols
Continous basal lamina
kidneys and intestines

299
Q

Discountinuous capillary

A

Discontinous endothelial cells separated by wide spaces
discontinous basal lamina
found in liver (proteins), bone marrow (WBC) , spleen (RBC)

300
Q

Compliance

A

Change in pressure for a given change in volume

301
Q

What happens to systolic and diastolic with a decreased compliance?

A

Decrease in aortic compliance results in an increaase in systolic and diastolic pressures. (ie. widening or increase in pulse pressure)

302
Q

Problems with low compliance system

A

Results in larger afterload, Increases O2 consumption, and is an independent risk factor for congestive heart failure

303
Q

Relation of the radius and trans-mural pressure

A

Compliance of the blood vessel wall decreases at higher volumes. B/c the load on the vascular wall is firrst borne by the elastin and smooth muscle and lastly by the collagen (lowest compliance)

304
Q

How does age affect aortic compliance?

A
  1. compliance decreases with age; less elastin and more collagen
  2. As compliance decreases, a given increase in volume elicits a larger increase in pressure
  3. less complian aorta results in wider pulse pressure and more cardiac work
  4. An increase in pulse pressure is an indpendent risk factor for the development of congestive heart failure
305
Q

What increases the arterial compliance?

A

Exercise

306
Q

Resistance vessels

A

Arteries exhibit a relatively constant low compliance throught the physiological range

307
Q

Capacitance vessels

A

Veins exhibit a relatively high compliance in the physiologically pressure, so veins can accomodate relatively large volumes of blood with little increase in pressure

308
Q

How is the compliance of veins in higher pressures

A

compliance is low, this allows saphenous veins to be used as coronary bypass grafts

309
Q

Pressure pulse

A

Travels down the aorta at 5 meter/s and incrases to about 10-15 m/s in small arteries.

310
Q

How fast does blood flow move?

A

1 m/s, radial pulse

311
Q

What determines the pressure pulse?

A

propagation of the pressure pulse wave depends on the physical characteristics of the vessel wall, especially the arterial compliance. As compliance decreases down the arterial tree, the velocity of propagation fo the pressure pulse increases.

312
Q

Mean arterial pressure =

A

Diastolic Pressure + 1/3 Pulse Pressure

313
Q

Determinants of Arterial Pressure

A

Physiological: Cardiac output, Peripheral resistance, Baroreceptor reflex, exercise, disease

Arterial blood volume, arterial compliance

314
Q

What pressure does cardiac output effect?

A

Systolic, regulated by autonomic nervouse

315
Q

What pressure does peripheral resistance affect?

A

Diastolic pressure

Regulated by local metabolic activity

316
Q

What pressures do arterial compliance effect?

A

Affects both systolic and diastolic pressures

317
Q

For a given arterial compliance, how does the arterial pressure change when you change the Peripheral resistance?

A

As resistance increases, both the systolic and the diastolic pressure increases (diastolic more)

318
Q

For a given resistance, how does the arterial pressure change with changing compliance?

A

Less compliance will creater a larger systolic and smaller diastolic. Ie. there will be a larger gap between systolic and diastolic

319
Q

Biggest factor affecting peripheral resistance

A

Arteriolar radius (remember r^4

320
Q

Draw the factors affecting total periperal resistance

A

Draw it

321
Q

Draw the effects of autonomic nervous activity on mean arterial pressure

A

Draw it

322
Q

Draw the Determinants of mean arterial blood pressure

A

Draw it over and over

323
Q

Different things governing the transcapillary fluid exchange

A
  1. oncotic pressure - osmotic pressure exerted by substances in the plasma
  2. capillary hydrostatic pressure
324
Q

Biggest determinant of oncotic pressure

A

Albumin, very high concentration and it’s charged, so brings Na as well

325
Q

Determinants of capillary hydrostatic pressure?

A

Arterial and Venous pressure

  • Arterial exerts small effect
  • venous exerts large effect b/c of little post-capillary resistance
  • Determined by the pre/post capillary resistance ratio
326
Q

What will cause a bigger increase in capillary hydrostatic pressure: increase of 5 to the pre or post capillary pressure?

A

Venous pressure will exert a greater increase in capillary hydrostatic pressure

327
Q

How does the lymphatics effect the interstitial fluid?

A

Lymphatics work by collecting and returning interstitial fluid to the circulatory system

328
Q

Structure of lymphatics

A
  • uniderictional flow of tissue fluid and protein back to the heart
  • valves, but thinner wall
  • non fenestrated endothelium, no basal lamina, no smooth muscle
  • large collecting vessels return lymphatic fluid to the subclavian veins
329
Q

What governs the lymph flow

A

capillary filtration
skeletal muscular activity
lymphatic unidirectional valves

330
Q

Clinical manifestations of edema

A

ankles, ascites, pulmonary edema

331
Q

What causes edema

A
  1. CHF
  2. Mechanical obstruction of venous return
  3. renal issues
  4. liver disease (lack of albumin)
  5. Burns - increases capillary permeability
332
Q

Basal tone

A

reference point for a vessel. The tone of a vessel under resting conditions without any extrinsic innervartion

333
Q

Resting sympathetic tone

A

amount of vascular constriction found under resting conditions as a result of tonic sympathetic nerve activity

334
Q

Active vs. passive mechanisms in vessels

A

Mechanisms induces a change in vascular resistnace away from the basal arterial tone
passive - induce a change in vascular resistnace back toward the basal arterial tone (basing just getting rid of sympathetic innervation)

335
Q

Alpha receptors

A

Located on vascular smooth muscle; causes vasoconstriction

Coronary and cerebral vessels have little sympathetic vasoconstricotr innervation

336
Q

Beta1 Receptors

A

Primary adrenergic receptor on cardiac muscle; stimulated heart rate and contractiltiy

337
Q

Beta 2 receptors

A

Secondary adrenergic receptor on cardiac muscle; stimulates heart rate and contractility;
Also located on vascular smooth muscle to cause vasodilation

338
Q

Are parasympathetic fivers on many tissues?

A

Innervate a limited number of blood vessels; cerebral, some viscera including splanhnic, genitalia, bladder, and large bowel. Causes vasodilation. Skeletal muscle and cutaneous vessesl are not innervated by parasympathetic nerves

339
Q

Baroreceptors

A

key role in short-term adjustments of bp
- walls of carotid sinus and aortic arch. Less vascular smooth muscle
- stretch recepotrs.
- Nerve firing increases with increases bp and decreases with decreasing bp
-

340
Q

What happens in baroreceptors with decrease in arterial pressure

A
  • stimulates sympathetic and inhibits parasympathetic nerve activity
  • peripheral vasoconstiction
  • increase in heart rate
  • increase in ventricular contractility
341
Q

Do the barareceptor feedback loop

A

Damn it

342
Q

Are baroreceptors more attuned to static or phasic pressures?

A

Much better with phasic

343
Q

What is the minimum pressure baroreceptors can sense?

A

50 mmHg

344
Q

What happens to barorceptor firing in hypertensive patients?

A

The receptors become less sensitive. Basically, it will create a new baseline.

345
Q

Chemoreceptor reflex

A

located similar to same place as baroreceptors. Activated by low arterial low PO2, high PCO2 and low arterial pH. Carried through IX and X Cn

  • Causes vasoconstriction and bradycardia
  • Goes through the medulla
346
Q

How does Co2 and O2 affect respiration?

A

Decreased O2 and Increased Co2 will cause a greater response in respiration thorugh the peripheral chemoreceptors

347
Q

Explain the renin-angiotensin aldosterone hormonal control of circulatory system

A

Long term regulation of BP
renin is from kidneys - helps to convert angiotensinogen to Ag1, eventually becomes Ag2 from ACE. AGII is most powerful vasoconstrictor, stimulates aldosterone, causes kidnes to reabsorb Na and pull water in
- causes thirst
- Designed to bring blood volume up to bring volume up

348
Q

Which resitance vessels work to control blood flow?

A

Arterioles
precapillary sphincters
metarterioles
venous resistance

349
Q

What governs the total peripheral resistance?

A

Vascular smooth muscle

350
Q

Autoregulation

A

intrinsic property of an organ or tissue to maintain constant blood flow despite changes in arterial perfusion pressure

351
Q

What happens to blood flow in normal physiological conditions when the arterial pressure increases?

A

The blood flow will increase; however, quickly decline back down to baseline

352
Q

What is the autoregulatory range

A

With increased resistance, blood flow will stay relatively constant until resistance exceeds the maximum range.

353
Q

What are the two primary mechanisms of autoregulation?

A

myogenic hypothesis

metabolic hypothesis

354
Q

Myogenic hypothesis

A

Vascular smooth muscle contracts in response to stretch and relaxes in response to a reduction in stretch
- increase in pressure causes an initial stretch of the vessel wall , which causes vasoconstriction, thus increased resistnace and decrease in flow

355
Q

Metabolic hypothesis of autoregulation

A

Metabolic activity produces metabolites that relax vascular smooth muscle. When pressure is increased there is a brief increase in blood flow which removes the inhibitory metabolites and allows the resistance vessels to constrict. THus, resistance icnreases and flow decreases

356
Q

Strong, weak, or no regulatory organs

A

strong - heart, brain, kidney, skeletal
weak - splanchnic
None- skin, lungs

357
Q

Does autoregulation utilize the endothelium?

A

No! When transmural pressure increases, the vessel will constrict. Even if the endothelium is removed, this will still happen

358
Q

What happens when the pressure gradient (flow) is increased but the transmural pressure is held constant? What controls this?

A

The vessels will dilate

- This is controlled by the release of EDRF or NO in response to shear stress

359
Q

Macro level metabolic regulation

A

blood flow in a given tisue is regulated by the metabolic activity of the tissue. Ie. Metabolites are released from tissue to cause dilation around the tissue in addition with a decrease in O2 delivery

360
Q

Active hyperemia

A

increased blood flow caused by enhanced tissue activity. Relies on interstitial osmolarity

361
Q

Reactive Hyperemia

A

Transient Increase of blood flow that follows a brief arterial occlusion. The longer the occlusion the greater the response. The response will be an overshoot

362
Q

What is the primary determinant and regulator of coronary artery blood flow?

A

Primary determinant - aortic pressure

Regulation - metabolic activity and changes in arteriolar resistance

363
Q

How does the LV tissue pressure effect coronary blood flow?

A

The left coronary blood flow is very influenced by LV tissue

At the beginning of systole the left coronary artery blood flow will actually decrease

364
Q

When is the maximal left coronary blood flow?

A

During early diasotle when tissue pressure is at 0

365
Q

When does most blood perfusion through the coronary system occur?

A

60-65% occurs during systole

366
Q

What vessels are more at risk for ischemia?

A

The endocardium is more at risk b/c the diastolic pressure is greater near the endocardium, so the vessels are more compressed

367
Q

Under normal conditions are the vessels in the endocardium at risk?

A

No, they will dilate
However, under abnormal conditions the greater endocardial tissue pressure can reduce coronary blood flow and produce subendocardial ischemia

368
Q

Describe the neural factors regulating coronary arteries

A
  • sympathetic adrenergic stimulation activates alpha receptors in the coronaries (weak vasoconstriction)
  • B1 receptors on pacemakers have strong vasodilation
  • Vagus can effect at normal constant rate
369
Q

What happens to coronary blood flow with increased myocardial metabolism?

A

Decreased resistance

thus, increased coronary blood flow

370
Q

What are the metabolic substrates for the heart?

A
  1. Fatty Acids (60%)
  2. Carbohydrates (35-40%)
  3. others
371
Q

Explain what it means that oxygen to the heart is flow limited?

A

The heart will extract 80% of the O2 which really cant be better. Thus only way to increase the heart oxygen is to increase the coronary blood flow
O2 consumption is directly related to the work of the heart

372
Q

Cardiac work

A

mean arterial pressure x systolic stroke volume

373
Q

Does pressure work or volume work consume more oxygen?

A

Pressure work

374
Q

Factors for supply of blood flow to the coronaries?

A 
diastolic perfusion pressure
Coronary vascular resistance
local metabolites
endothelial factors
neural innervations
375
Q

Factors for oxygen demand in the coronarie?

A
  1. Afterload
  2. Heart Rate
  3. Contractility
376
Q

What can adenosine be used for?

A

Causes quick vasodilation which also goes away very quickly

377
Q

Collateral circulation

A
  • In response to gradual obstruction of a coronary artery collateral vessels can grow enough to restore an adequate blood supply to the myocardium
378
Q

Coronary steal

A

If there are two vascular beds and one starts developing a plaque, it will dilate. However, if during exercise everything needs to dilate, only one of the two beds will be able to as the other has already dilated

379
Q

What is the largest vascular bed in the body?

A

Skeletal muscle. Take about 20% of cardiac output

380
Q

How much is normal blood flow in skeletal muscle during resting conditions?exercise?

A

3 ml/min

20x

381
Q

Active hyperemia

A

Increase in blood flow due to metabolic activity

382
Q

How does skeletal muscle regulate large or small blood flow?

A

has a large resting tone from interplay between vasoconstricotr and vasodilator influences. In rest, vasoconstrictor influences dominate, whereas during muscle contraction, vasodilator influences dominate ton increase oxygen deliver

383
Q

On average, what happens to resistance during exercise?

A

Profound reduction

384
Q

How does isometric contraction effect the vascular compression/

A

It is sustained, thus very little blood flow.

Further, vascular resistance increases and cardiac output rises

385
Q

How does acetylcholine effect skeletal muscle?

A

Causes vasodilation by acting on muscarinic receptors on endotherlial cells coupled to NO

386
Q

How does epinephrine effect skeletal muscle?

A

Comes from adrenal medulla and causes vasodilation at low concentrations through activation of B2 adrenergics.

387
Q

Does the brain have lymphatic vessels?

A

No

388
Q

What is the least tolerant organ to ischemia?

A

Brain, Interruption of cerebral blood flow for as little as 5 sec results in loss of consciousness and ischemia lasting a few minutes results in irreversible brain damage

389
Q

What gives the blood brain barrier it’s attributes?

A

Endothelial cell tight junctions, basement membrane, neuroglial processes and metabolic enzymes

390
Q

What can cross the blood brain barrier?

A

Lipid soluble substances such as O2, CO2, ethanol, steroid hormones

391
Q

What can’t pass through the BBB?

A

MW > 500 daltons

392
Q

What factors affect the cerebral blood flow?

A 
Autoregulation
Tissue Pressure
Metabolism
Autonomic nervous system
Cushing's response
393
Q

Is blood flow rate the same everywhere in the brain?

A

Autoregulation will maintain a consisten blood flow to the brain; however, regional blood flow can increase during high activity

394
Q

What is the normal range for cerebral perfusion pressure?

A

80-100 mm Hg

395
Q

What happens to the autoregulator curve in the hypertensive state?

A

It will shift to the right

396
Q

Cerebral perfusion pressure

A

Mean arterial pressure - intracranial venous pressure

397
Q

What happens to blood if there is increased cerebral perfusion pressure?

A

The blood will be pushed elsewhere, causing ischemic region

398
Q

What happens as CSF pressure increases?

A

Cerebral blood flow will decrease very rapidly

399
Q

What is the Monro-Kellie Doctrine?

A

Brain volume + Cerebral vascular volume + CSF volume = constant

When one of the things increases there must be a compensatory decrease

400
Q

How is blood flow related to pH?

A

Decrease pH causes vasodilation and increased blood flow

401
Q

How does blood pH effect cerebral blood flow?

A

Little effect b/c H+ can’t cross BBB

However, pH due to changes in CO2 can rapidly change cerebral blood flow b/c CO2 can cross the BBB

402
Q

How does CO2 effect cerebral blood flow?

A

lowers pH causing vasodilation. Conversely, decrease in PCO2 raises pH and causes vasoconstriction

403
Q

fMRI

A

looks at the ratio of deoxy to oxygenated hemoglobin in blood, which in turn is a function of local arterial autoregulation or vasodilation. Allows determination in unanesthetized patients of the brain’s metabolic activity during different tasks

404
Q

3 types of vasodilators

A

Adenosine
K
NO

405
Q

Autonomic nervous control of the cerebral blood flow

A

para - division of the facial nerve carries parasympathetic innervation to cerebral vessels
symp - exerts minimal vasoconstriction. Baroreceptor reflex has little effect
- Local metabolic activity is the primary control, not neural

406
Q

Cushing response

A

elevated intracranial pressure causes a decreased cerebral perfusion
- causes stimultion of vasomotor cetners in the medulla that increase sympathetic nerve activity
causes high systemic arterial blood pressure
- Finally, the IC pressure activates para nerve activity which decreases heart rate

407
Q

Portal hypertension

A

Can result from increases in either the vena cava pressure (CHF) or the hepatic vascular resistance

408
Q

Portal hypertension

A

> 25 mm Hg can lead to abdominal edema formation or ascites. If pressure increases further, portal blood flows through and dilates portal anastomoses with systemic veins in the lower esophagus, stomach, and rectum

Function of the Body: Section 1 (1 decks)

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