Midterm 2- Cardio Flashcards
(203 cards)
1
Q
What are the 4 principle functions of heart and its role as Transport system?
A
a. Transprot oxygen and nutrients to various tissues
b. Transport carbon dioxide and waste products of metabolism from tissue to environment
c. Regualte body temp (by transporting excess heat out of body)
d. Transport and distribute hormones and other substances
2
Q
Components of transport system?
A
a. central pump= Heart
b. closed system of blood vessels
c. fluid medium blood through which various substances are transported
3
Q
What is pulmonary circulation?
A
- carries blood to and from the lungs
- provides exchange of gases between atmosphere and blood
Right atrium - right ventricle - pulmonary artery- pulmonary capillary - pick up oxygen and remove SOME carbon dioxide - pulmonary vein- left artium - left ventricle- aorta
4
Q
What is systemic circulation?
A
carries blood to and from the rest of the body
Aorta- arteries - arterioles- capillaries - exchange vessels where oxygen and nutrients diffuse into tissue and carbon dioxide and waste products are picked up - venules - veins- right atrium
5
Q
Series circuit and examples
A
in series to heart, eg. PTC and GC kidney, liver and digestive system
6
Q
Parallel circuit and name the advangtages and example
A
- vascular capillary parallel to heart
Advantages:
1. amount of blood flow to individual vascualr beds can be controlled separately by dilating or constricting the artery supplying vascualar bed
2. relatively low resistance to blood flow; lowers the pressure requirment for blood flow thus decreasing work load on heart
Examples:
deliever increase oxygen to muscles and decreae to kidney, liver and GI
7
Q
What is the total blood volume?
A
5L
8
Q
What is the percentage distribution of blood?
A
Heart and pulmonary circualtion = 15%
Systemic Arterial circulation = 10%
Systemic Arterial capillary= 5%
Systemic veins = 70%
9
Q
Draw a diagram of the circulation path of blood through the heart.
A
Refer to Cardio page 2
10
Q
Describe the relationship between valves and tendones?
A
valves have tendonae attached to pipillary muscles.
- when ventricle contract, the valves are just leaflets if they were to flop the other way, it would allow blood back to atrium.
- Chorea tendonea are being pulled by pipillary muscles to close the valve when the ventricle is pushing up, to inhibit the blood from going back to atrium.
11
Q
What are the two types of myocardial cells?
A
Cardiac contractile cells and specilized excitatory/conducting cells
12
Q
Where are cardiac contractile cells found?
A
found in atria and ventricular muscles
13
Q
Similarities of cardiac contractile cells to skeletal muscle
A
- straited and contain actin and myosin
- contraction invovles sliding of myofilament
- contraction invovles calcium
- multinucleated
14
Q
What are the differences between cardiac cells and skeletal muscle?
A
- shorter, branched and arranged in series with each other
- each fiber is a complete unit surrounded by cell memrbane -> sarcolemma
- 1/3 of the volume is occupied by mitocondria to extract 80% of oxygen from blood
- cardiac cells are arranged in series with each other and contain intercalated disc- where the ends of two cardiac cells meet and join by gap junctions to allow free movement of ionic currents
15
Q
What is functional syncytium?
A
when 1 cardiac cell contracts, they all contract
16
Q
What are the two separate functional syncytia? and how are they separated? and why is the separation important?
A
Atrial syncytium and Ventricular syncytium. They are separated by atrioventricular ring that surrounds the valvular opening between atria and ventricles
- AP can be conducted from trial to ventricular by special conduction system- AV node and bundle of his
- divison is important to allow atria to contract a short time ahead of ventricular
17
Q
What are speciliazed excitatory and conducting cells?
A
They are self-excitable cells capable of spontanneously generating APs.
- rapidly conduct APs through the heart
- provide self-excitatory system for heart to generate impulses and transmission system for rapid conduction
18
Q
What is the speed of AP between neural and cardiac?
A
Neural AP is in ms and cardiac AP is in sec, so its slower
19
Q
What are the two types of excitatory nodal cells and conducting cells?
A
Excitatory: Sinoatrial node and Atrioventricular node
Conducting: Bundle of His and Purkinje fibers
20
Q
Where do the impulses originate and what is a normal heart rate?
A
Impulses normally orginate in SA located in the upper posterior wall of right atrium. Most cells of the heart have the capability of self-excitation = can spontaneously generate AP. The normal HR is 72bpm
21
Q
What controls the HR?
A
SA controls the HR and is the fastest self-excitation in the heart, called the pacemaker of the cell
22
Q
What is the diff between SA node AP and ventricular Muscle AP?
A
SA node AP: slow response AP because of its slow rate of depolarization
Ventricular Muscle AP: fast response AP
- Difference due to the diff cardiac cell utalizing special ion channel to produce distinctive AP
23
Q
What are the characteristics of SA Node responsible for self-excitation? How do these characteristics determine its role in the heart?
A
- When in diastole, the cells of SA node have greatest NA and Ca permeability thus positive inward current.
- K permeability of SA node declines during diastole- relaxation phase. Due to the properties, SA node does not have a stable resulting memrbaen potential - prepotential or pacemaker potential.
24
Q
What is the memrbaen potential of SA node and how does it compare to the ventricular fiber?
A
The memrbane varies from -60mV to 20mV, and has a threshold voltage of -40mV. In comparison, the max negativity of ventricular fiber is -90mV to 20 mV
25
List the stages of SA node and draw the diagram.
1. Slow depolarization (spontaneous)
- greater permeability to Na (funny channels which open at -60mV)
- allows Na into the cell and Ca (via T-type VG and some slow L-type Ca channels)
- allow Ca to slowly enter the cell
- decrease K permeability (outward K movement decreases overtime
- Pre-potential
2. Depolarization
- at threshold -40mV, Na funny cahnnels and T-type Ca VG channels closed
- ALL L-type Ca VG channels open causing the depolarizing phase of SA nodal AP and membrane to reach 20mV.
- Ca2+ flows in (slowly = slow response AP)
3.Repolarization
- slow L-type calcium VG channels begin closing
- K VG channels open leading to increased outward K current
- large amount of K diffuses out and membrane returns to -60mV
Cycle repeats
- more and more K VG channels begin to close decreasing outward K current and Na and Ca leaking in causes slow depolarization to theshold
26
What is the slow depolarization step in SA node AP?
1. Slow depolarization (spontaneous)
- greater permeability to Na (funny channels which open at -60mV)
- allows Na into the cell and Ca (via T-type VG and some slow L-type Ca channels)
- allow Ca to slowly enter the cell
- decrease K permeability (outward K movement decreases overtime
- Pre-potential
27
What is the depolarization phase in SA node AP?
2. Depolarization
- at threshold -40mV, Na funny cahnnels and T-type Ca VG channels closed
- ALL L-type Ca VG channels open causing the depolarizing phase of SA nodal AP and membrane to reach 20mV.
- Ca2+ flows in (slowly = slow response AP)
28
What is the repolarization phase in SA node AP? How does the cycle repeat?
3.Repolarization
- slow L-type calcium VG channels begin closing
- K VG channels open leading to increased outward K current
- large amount of K diffuses out and membrane returns to -60mV
Cycle repeats
- more and more K VG channels begin to close decreasing outward K current and Na and Ca leaking in causes slow depolarization to theshold
29
What determines the HR in SA node?
The rthythmic generation of AP determines the HR
30
What are the two ways that the rat eof AP generated by SA node can be altered by?
a. Change the slop of the prepotential (diastole depolarization - make slope steeper or longer (slow HR)
b. Change the memrbane potential from -60mV ie hyperpolarization - repolarize to -70 or -80 mV so it takes longer to reach threshold
31
Draw the diagram of VG K channels, Funny channel VG and ligand gated Na and T-type Ca VG channel and L-type Ca VG channel
Look at Cardio Page 2 back side
32
What does the VG K channel contribute to in SA node AP?
Prepotential and repolarization phase of SA Nodal AP
33
What does the Funny channel Na contribute to in SA node AP?
Pre-potential- inward Na current crrated by funny channel NA along with T-type Ca and small L-type slow channel
34
What does the Ca channel contribute to in SA node AP?
Depolarization - slow L-type Ca channel
35
What are the steps to the conducting system of the Heart?
1. SA nodal fibers fuse with surrounding atrial msucle ffiber therefore impulses generated by SA node spread throughout Atria
- Anterior Interatrial myocardial band conduct impulses from SA node to left atrium
2. Atrial contractile cells AP propogates from top to bottom atrium. Do not want AP to propogate from atrial to ventricular cells directly because then the ventricels would contract from top- down pushing the blood down
- want the ventricle to contract down- up
Atrioventricualr Ring- bundle of connective tissue
- electrically isolate atria from the ventricle (block AP)
3. Anterior, Middle, and posterior internodal pathway
- conduct impulses from SA node and AV node
- band consist of ordinary myocardial cells and specialized conducting fibers
4. AV node
- slows down the AP to ensure atria has finished contracting before ventricle contracts
5. The impulses are transmitted from AV node to bundle of his (takes AP to apex of heart)
- divides into Right Branch and left Branch bundle of His
6. AP travels from Bundle of His -> purkinje fibers
- transmit the impulses to ventricualr muscles fiber
- APEX contractile cells - down -> ventricle contractile cells up - HIGHLY coordinated
36
Draw the diagram of Conducting System of Heart
Cardio Page 3 Conducting System of Heart
37
Write the Conduction velocity for SA node, Atrial Muscle, AV node, Bundle of His, Purkinje Fiber, and Ventricle.
```
SA node- 0.05
Atrial Muscle - 0.4-1.0
AV Node - 0.05
Bundle of His- 1.0
Purkinje Fiber- 2.0 - 4.0
Ventricle- 0.4-1.0
```
38
Explain the conduction of impulse throughout the Heart
It is the velocity of impulse conduction in various part (NOT GENERATION of AP)
- After a moderate velocity of conduction in the atria, the velocity slows down on AV node.
- At AV node, there is a delay in transmitting, the impulse from atria -> ventricle
- Allows for atria to contract and empty blood into ventricles before ventriclar contraction begins
- Purkinje system conduction velocity increase
- allows for immediate trnamission throughout ventricular system
- after impulse enters Bundle of His, it takes 0.6s to excite entire ventricualr muscle
- ventricualr musclce remains contracted for 0.3 sec.
- causes both centricles to contract at the same time
39
If SA node is damaged, what happens to HR?
- other parts, particularly AV node and Purkinje fiber can initiate rhythmic contract
- AV node discharge at 40-60 times/min
- Purkinje fiber at 15-40 times/min
SA node discharge at 100 times/ min
40
How can the activity of Heart be recorded?
- The body fluids are good conductors of electricity
- Heart is emerged in conducting fluids
- cardiac impulse generated by SA node pass through heart, surrounding tissues and surface of body
- electrodes on skin (opposite side of heart) can detect electrical potentials generated by heart
41
What is ECG?
sum of all electrical events in the heart. Depolarizing and Repolarizing
42
Draw the diagram for ECG
Cario Page 3 back side
43
```
What is :
P-Wave
QRS Complex
T Wave
U wave
```
P-wave- depolarization of atria muscles
QRS complex- rapid depolarization of both ventricles; ventricles have large muscle mass than atria so QRS has a larger amplitude than P-wave
T-wave- repolarization of ventricles
*repolarization of atria is not shown because it is small and obstructed by QRS complex
U-wave- Repolarization of Papillary muscles in ventricle
44
What is PR Interval and QRS Interval of ECG?
PR Interval:
- the time it takes AP to travel from Sa node through AV node to ventricles
- good indicator of AV node function
- PR interval decreases as HR increases
Atrial depolarization and conduction through AV node
QRS Interval:
- indication of speed of conduction through bundle of His- Purkinje system
Normal QRS- fast AP propogation through His-Purkinje
Wide QRS- slow AP may be jumping to ventricle through antoher pathway- Wolf-Parkinson - White syndrome
45
What happens to PR interval as HR increases?
| What happens to QRS as it gets wider and the name of the syndrome?
PR interval decreases as HR increases
| QRS- slow AP may be jumping to ventricle through antoher pathway- Wolf-Parkinson - White syndrome
46
What is Wolf-Parkinson White syndrome?
secondary pathway of passage of AP from atrium to venticle due to damage in AV node
- shortening of PR interval and longer QRS complex
47
If there is a 64 year old male with shortness of breath, light headed with severe chest pain; HR is 35 bpm, what is the problem? What is the treatment?
Myocardial infarction
- the conduction system, bundle of his or branches has been damaged so AP cannot propogate down
- the hR is slower because other areas of the heart takes over so bundle of his is going to take over and start the AP at slower HR
Treatment:
- implant a pacemaker that will monitor the output of SA node and fire an AP
48
Draw the AP for the ventricular contractile cells
Look at Lecture 3 of Cardio
49
Describe the AP of ventriculaar contracile cells
AP started in SA node and propogates to and from ventricular cells to ventricular cells
Depolarization:
- current from neighbouring cell depolarize cells (via gap junctions)
- open fast VG Na channels and Na enters very rapidly (fast inward motion)
- m.p reachest 20mV
Rapid Repolarization:
- Na+ permeability decreases (fast Na channels close)
- Cl- channels open and Cholride flows in while VG K channels open and K moves out- repolarization
Plateau Phase:
-AP opens ALL L-type slow Ca channels so calcium moves in slowly causing slow inward current
- this inward calcium current almost balances the outward K current
- Result is a relatively stable membrane potential "Plateau phase"
Restoration of resting potential:
- Slow L type calcium channels begin closing
- inward movement of Ca2+ decrease while K continues to move outward
Resting Potential:
- mp reaches -90mV
50
What is excitation-Contraction coupling?
AP on contractile cells lead to release of calcium from SR causing muscle contraction
51
What is the duration of AP in ventricular contractile cells?
300ms
52
What is similar with excitation-contraction coupling in heart and skeletal muscles?
AP on cardiac cell membrane (sarcolemma) spreads to T-tubule
| - depolarization of T-tubules causes release of calcium from SR into sarcoplasm
53
Describe the ECC in skeletal muscles
1. AP on the msucle cell travels down the T-tubule
2. Dihydropyridine (DHP) receptor/Cal channel (voltage sensor) on T-tubule changes conformation
3. DHP receptor opens ryanodine receptor (calcium channel) on SR which is directly physcially linked
4. Calcium is released from terminal cisternar of the SR
54
What is different from skeletal muscles?
- Extracellular calcium enters sarcoplasm during depolarization of sarcolemma
- the ca interacts with SR to cause further release of calcium from SR- calcium induced calcium release
- DHP in skeletal muscel is directly linked to SR while DHPR (slow l-type calcium chennales) is not directly linked
55
How can free intracellular calcium be increased in the heart?
a. depolarization induced calcium influx from ECF through slow L-type calcium channels (DHPR)
- directly interact with myofibrils for contraction
- DHPR/calcium cahnnels
b. Ca can enter through Na/Ca exchanger (pump is bidirectional) and switches when memrbaen potential is positive and Na conc is high
When would Na conc be high?
- during depolarization phase
c. Extracellular calcium induced calcium reelase
- calcium that entered through slow L-type calcium cahnnel and Na/Ca exchanger - can open Ryanodine on SR
d. Intracellular calcium induced calcium reelase from SR
- physical interaction of intracellular calcium with other ryanodine cahnnels on SR opens more channels causing Calcium release
56
Why is ECF calcium essential?
- essential for triggering calcium release from SR
- intracellualr calcium is increased by 1000 times
- the amount that enters through L-type is small comparerd to that is released by SR
- maintain adequeate levels of intracellular calcium stores over the long run
- essential for cardiac contraction
57
How does cardiac muscle contract after calcium is released in sarcoplasm?
1. calcium binds troponin
2. Troponin pulls tropomyosin off myosin binding sites
3. Myosin attaches to actin-cross bridge
4. powerstroke occurs
5. sliding of myofilaments
58
How does muscle relaxation occur?
Relaxation is caused by lowering the calcium intracellualrly.
a. 80% of the intracellular calcium is actively pumped back into SR by calcium ATPase (against conc gradient)
b. Calcium is actively pumped out of cell into ECF by similar calcium ATPase- 5%
c. Na/Ca exchanger pumps 3Na in for 1 calcium out (15%) -> activity depends on Na conc and Ca conc intracellularly
59
How is the relationship between the AP and resulting muscle contraction in heart diff from motor unit?
1. contraction/mechanical response of muscle begns jsut after the start of depolarization and lasts 300 ms.
2. Response of the cardiac muscle occupies most of the absolute refractory period of AP
3. When the refractory period ends, more than 75% of contractile response is over; the muscle has already relaxed
therefore, the summation of twitches and a resulting tetanic type of contraction seen in skeletal muscle cannot occur due to long plateau, refracctory period and long duration in cardiac muscles
60
Describe the cardiac cycle
The cardiac cycle consist of ventricular diastole (longer) and systole.
- cardiac cycle is initiated by SA node (spontaneous generation of AP
- the impulses spread throughout atria and conducted into AV node and than into ventricles - well coordinated propogation of AP
- AP leads to pressure changes that cause opening and closing of valves
61
What are the 7 stages of the cardiac cycle?
1. Atrial systole
2. Isovolumetric contraction
3. Ejection period (Rapid)
4. Protodiastole
5. Isovolumentric Relaxation
6. Rapid inflow
6. Diastasis
62
What happens in the cardiac cycle during atrial systole?
- P-wave -> atrial depolarization leading to atrial contraction
- Atrial pressure is greater than ventricular pressure- AV valves were already open
- Last 30% of ventricular filling
- Atria contracts-> AV valves are already opened so blood flows into the ventricle (last 30%)
- Eng diastolic volume- volume of blood in the ventricle at the end of diastole (EDV)
63
What happens in the cardiac cycle during isovolumetric contraction?
- volume of blood in ventricle is not changing even though ventricle is contracting
- QRS complex -> ventricle beings contracting -> pressure in ventricle increases
- ventricle pressure > atrial pressure- AV valve close -> 1st heart sound
- with all valves closed, there is no change in volume (ventricular pressure is less than aortic pressure)
- Left atrial pressure increases because the ventricle pressure pushes on AV valve increasing the atrial presssure (papillary muscle keeps the AV valve from opening/flipping to the other side)
64
What happens in the cardiac cycle during ejection period?
- Ventrile continue to contact
- Ventricle pressure > aortic pressure -> aortic valve opsn and blood leaves ventricle
- ventrile volume decreases
- begining of T wave- repolarization of ventricle
65
What happens in the cardiac cycle during Protodiastole
- ventricles just begining to relax
- ventricle pressure starts to fall
- aortic pressure is higher than ventricular pressure because blood is still moving into aorta due to inertia (aortic valve still open)
- little blood leaves the ventricles (not all the bloodi n ventricle leaves during phase 3-4, blood still remains - 90 ml left- End systolic volume ESV
66
What happens in the cardiac cycle during isovolumentric relaxation?
- ventricle continue to relax
- ventricualr pressure durther drops
- blood in aorta reverses direction and causes aortic valve to close-> 2nd heart sound; aortic pressure higher (incisura) blood that is coming to ventrile hits the valve and it pushes the blood out
- venricular pressure higher than atrial pressure- no change in ventricular volume, atrial pressure increases
67
What happens in the cardiac cycle during rapid inflow?
Ventricle still relaxing
- ventricle pressure is less than atrial pressure- causes AV valve to open
- blood rapidly enters ventricles (most of ventricular filling
68
What happens in the cardiac cycle during diastasis
- occupies middle 1/3 of ventricualr diastole
- ventricle still relaxed
- vent pressure < atrial pressure so AV valve still open
- bblood enters ventricles but more slowly
69
What are the three heart sounds? and why are they casued?
First sound- Lub
- results from vibration within the blood and muscle wall associated with the sudden back of flow reversal by valves
- at the beginning of ventricular contraction
- block of reverse blood flow due to closure of AV valves
Second Heart sound- Dub
- caused by vibration within the blood, muscle wall, and aorta associated with the sudden block of flow reversal by aortic valve
- at the end of ventricualr systole
Third heart sound
- blood hitting ventricle
- often not heard, only in children
70
What is cardiac output? Write the equation.
It is the amount of blood pumped by the ventricle/min. CO = HR * stroke volume
SV- amount of blood ejected from ventricle when it contracts
71
What is CO matched to and what is the range in the body and
CO is matched to the oxygen demands of the body. At rest, CO=5l/min anad it can inccrease to 20L-40L/min
72
How can you calciulate CO at rest?
= 72bpm * 70ml = 5l/min- total blood volume of an avg individual is circualted rougly every min at rest
73
describe the relationship of CO in right and left ventricle
The output in right ventricle is the same as left ventricle because systemic venous blood eturns to the right side of the heart
74
Which three organs recieve the most CO and why?
Brain, Liver and kidney
Liver- support its high level of metabolic activity
Brain- provide nutrient and prevent H and CO2 concentration from being too high in body fluids
Kidney- adequate excretion to maintain a safe body fluid
inactive muscles have low metabolic rate but active muscle have high metabolic rate and can increase sa much as 50 time and blood flow increases by 20 times
75
What are the factors controlling cardiac output?
- depends on fitness, CO increases during exercise to 20L/min in untrained individuals and as high as 40L/min in highly trained individuals
- increase CO to match the demands of the tissues in the body
- untrained have increase HR whereas trained individauls can increase HR and SV during exercise
76
what is the equation of CO?
CO = HR * SV
77
How do you control CO by changing HR?
- HR is set spontaneous generation of AP in SA nodde- prepotential- any change in the rate of depolarization threshold will change the HR
HR can be altered by:
a. changing the slope of prepotential
b. hyperpolarizing the memrbane potential
HR is primarily controlled by ANS
SNS- increase in HR and increase in CO
PNS- decrease HR and decrease CO
78
Recall the neurotransmitters in ANS:
1. pregang neurons of PNS and SNS secrete ACH -> cholinergic neurons which binds nicotine receptors
2. Post gang neurons of PNS also secrete ACH- PNS is totally cholinergic, receptors are muscarinic and can be blocked by atrophine
3. Most post gang neurosn of SNS secrete norepinephrine (NE) which acts on adrenergic receptors- affects smooth, cardiac muscles and glands
4. Post gang neurons of SNS secrete Ach instead of NE exceptions include:
a. Post gang sympathetic fiber to sweat glands and pilorector muscles
b. Post gang sympathetic cholingergic vasodilator nerve to blood vessels of skeletal muscle which secrete Aach
c. Symp pre gang fiber to adrenal medulla secrete Ach which binds to nicotine to release Epi and NonEpi (20%)
79
Where are the PNS and SNS nerves distributed in the heart to control HR?
PNS nerves are distributed mainly to SA and Av nodes and have a small indirect effect on atrial and ventricular muscles
SNS nerves are distributed to SA and AC node with a strong input to ventricular muscles.
80
What are the effects of PNS vagal stimulation on the heart rate and heart?
1. decreases GR- negative chronotropic response by decreasing the SA node activity
2. Decrease AP conduction through AV node
3. Decreasse force of contraction slightly- negative inotropic effect
81
What is the mechanism of Para Symp Effects on the heart?
Ach is released by cholinergic post gang which binds muscarinic recpetors
- this opens special K cahnnel to increase K permeability- hyperpolarize the cell
- decrease the calcium permeability by slowing the opening of L-type calcium channels
- results in more K leaving and less calcium entering SA nodal cells
- decrease slope of prepotential
- cause longer time to reach threshold, which would decrease HR
- decrease AP conduction through AV node
82
What are the effects of Sympathetic stimulation on the heart?
1. increase HR- positive chronotropic response
2. Increase AP conduction rate through AV node
3. Increase force of contraction (positive inotropic response - strength of contraction)
83
What is the mechanism of sympathetic tone on heart rate?
Non-epi released by sympathethic nerve ending bind B1 adrenergic receptors
- increase Na permeability funny channels
- increase calcium permeability by opening slow L-type calcium channels
In SA node- increase ca and Na permeability increase slope of prepotential
In AV node: increase Na and Ca permeability which makes it easier for each fiber to excite the succeeding fiber
- decreases conduction time between atria and ventricle (reach threshold faster, increase HR)
- it doesn't affect repolarization, so it still reaches -50mV
84
Whicch ANS system do you activate when HR is < 100bpm, = 100bpm, or > 100bpm?
For heart rate < 100 bpm- activte PNS
- at rest (70bpm), there is always PNS activity- vagal tone
- the mroe you activate the PNS, the lower the HR
FOr Heart rate = 100bpm, no PNS or SNS activated
- hearts own intrinsic rate set by SA node
FOr heart rate > 100 bpm, activate the SNS
- the mroe you activate the SNS, the higher the HR
85
What is the Maximal HR formula?
MaxHR=220-age
86
How can you change the CO?
by changing the HR or stroke volume
87
What is stroke volume?
amount of blood ejected by the ventricle on each contraction
88
What is the formula for stroke volume?
SV = EDV - SDV
89
What is EDV and SDV
EDV- volume of blood left in the ventricle at end of ventricular diastole- just before the ventricle contracts
ESV- volume of blood in left ventricle at the end of ventricular systole- just after ventricle is contracted
90
What are the three major factors that control strove volume?
1. Input from Autonomic Nervous system
2. Preload- realted to EDV
3. Afterload
91
How can you control the Stroke volumethrough iput from ANS SNS stimulation?
1. Norepi acts on B1 receptors on contractile cells
- increase calcium entry through L-type calcium cahnnels
- increase force of contraction ECC
- increase SV, CO
2. Release Ach from pre gang neurons onto medulla that reelase EPi and nonepi that act on B1-adrenergic receptors
- increase HR
- Increase contractility of heart (increase Ca entry)
- increase stroke volume
- increase CO
92
How can heart transplant patient increasae HR and SV during physical activity if heart is not attached to autonomic nerves?
Hormones that activate the sympathetic nervous system
93
How does the PNS stimulation affect the Stroke Volume to change CO?
1. caused by removal of all SNS activity, decrease SV
2. Left vagus nerve innervates left ventricle:
- closes some L-type calcium cahnnels
- decrease Ca entry into contractile cells
- decrease force of contraction
- decrease SV
94
How can you control stroke volume through cahnges in preload?
Preload- extent of filling the heart before contraction
- this load comes from blood in the ventricle- the more the blood in the ventricle, the more "loaded" the ventricels are with blood
- "load " on the heart before it contracts
- it is directly realted to EDV
- increase in EDV is increased preload, which causes increase force of contraction of ventricle and increasae stroke volume
95
SHow with a diagram how increase EDV will result in increase SV
Cardio page 7 back side
96
Describe the mechanism how increae EDV will result in increase force of contraction
- whe nthe EDV is increased, there is more blood in ventricles, so ventricles become stretched (enlarged)
- the legnth of ventricuar muscle fiber increases
- stretched muscle develosp a greater contractile force due to max overlap of actin and myosin
- increase foce propriotional to number of cross bridges
- max overlap between actin and myosin occurs only when muscle is stretched to its max physiolgoical dimensions
- stretching may cause stretch sensitive calcium cellsn and inccrease affinity of calcium for troponin
- more extracellular calcium enters cardiac contractile celsl and troponin has increase affinity for calcium when sarcomeres are longer
- at resting heart, you start at Low EDV thin filament bumping in M-line , interfering with formation of cross bridges
- fill heart with more blood would stretch the ventricle thus getting optimal overlap -> more forceful contration
97
What is frank-starling law of heart?
- the greater the heart is filled during diastole, the greater blood pumped during systole
- ensures quality of right and left ventricular pumping. ie, if one ventricle pumps a large amount of blood, the venous return to the other ventricle is increased.
98
What are the three ways to increase EDV in ventricle?
1. muscle pump
2. respiratory pump
3. ANS
99
How can you increase EDV using muscle pump?
- Rhythmic (muscle contracting and relaxing) contraction
- intramuscular pressure exerted on veins by surrounding msucles to push blood through one-way valve of veins, returning blood to heart
- pumping actions keep blodod from pooling in lower limp
- individuals standing still for extended period of time- > experience reduced venous return to heart and lower blood pressure- hypotension
- increase venous return by muscle pump increae EDV- increase SV and increase CO
100
How do you increase EDV using respiratory pump?
- during physical activity, you expand the ribcage to increas inhalation
- ocauses intrathoracic pressure (pressure in chest cavity) to drop, so that will pull air into your lungs
- drop in pressure in chest cavity, pulls the blood back to heart (right atrium) and increases venous return- incrase EDV, SV and CO
101
How can you increase EDV with ANS?
SNS causes sligh vasoconstriction- smooth muscle in the walls of veins increase venomotor tone causing them to constrict
- increase central venous pressure
- incrrease venous return
- increase EDV, SV and CO
102
What is the effect of afterload on SV?
afterload- resistance against which ventricle pump blood (ventricular wall stress during systole)
- the pressure in aorta during systole is the afterload encountered by left ventricle- ventricle has to exceed the pressure in aorta to open the aortic valve
- the pressure in pulmonary arteryduring systole is the afterload encounrted by right ventricle
Left-ventricle- amount of blood it ejects- stroke volume
- in order to ejet blood, there is a period of time (isovolum ventricle contraction phase) = no change in ventricular volume because ventricle start to contract and all valves are closed
- in order to open aortic valve, te pressure inside the ventricle has to be above the valve
- therefore, the pressure in aorta is afterload that must be exceeded to open valve
103
What happens to the SV when you pick up something haeavy?
- The Bp rises, aortic pressure increases (After load increased)]0 left ventricle has to generate more pressure to open aortic valve to eject blood
- ncrease duration of isometric contraction
- once entricualr pressure exceeds aortic pressure, aortic valve open and blood is ejected
- ejection phase is shortened because ventricle would begin relaxing, less tiem for blood to get ejected, thus less stroke volume
104
How can heart componsate for SV
- increasae EDV
105
What type of vessels are arteries, capillaries and veins?
Arteries- distribution vessles
Capillary- exchange vessels
Veins- collection vessles
106
Determine the cross sectional area and velocity of blood flow in systemic circulation
- consecutive branches of arterial system becomes smaller and smaller
- the proliferation of more and more blood vessel leads to massive increase in total cross-sectional area
- same total blood flow (l/min) passes each level
Blood veocity is slightly decreased
Velocity- how fast the blood is flowing through each situation
- velocity in singel vessel is high
Cross sectional area:
- total cross sectional area of aorta is very small
- whiel vessels are becoming smalelr and smalelr in diameter, and increasing in total number, this increases total cross-sectional area of these vessels
- highest in capilalries becasue there are so many of them
Mean velocity:
- velocity in a single vessel is high
- highest in aorta
107
Describe the diameter of the vessels
- vena cava is larger in diameter than aorta (also has lower blood velocity)
smallest are capilalry
108
What makes capillaries good for exchange?
- smallest blood mean velocity
- highest surface area
- shortest dffusion distance
- exchange takes palce
109
Describe the pressure throughout the systemic circulation and draw the diagram
- there is fall in pressure in each aprt of the systemic circulation which is directly prop to vascular resistance
- most of the resistance comes from friction that the blood encounters as it moves along the inside wall fo the vessel
Aorta:
- very little resistance to blood flow so pressure remains high
Small arteries:
- fall in pressure begins where the resistance to flow begin to slightly increases
Arterioles
- the greatest resistance to flow accounting for about half the ressitance in entire systemic circulation; pressure decrease about 45-50mmHg
- pressure in blood which leaves the arterioles to neter capilalries is only 40 mmHg
Capilalries:
- the pressure drop is about 20 mmHG
Venous circulation
- small but significant amount of resistance occurs in the venous side of circulation
- by the time blood reaches the right atrium, the pressure approaches 0 mmHg
110
What is systolic pressure and diastolic pressure?
Systolic pressure- related to force of cardiac contraction
| Diastolic pressure- related to resistance the blood as it flows through blood vessel
111
pressure drop is directly proportional to?
Vascular resistance
112
What is teh total peripheral resisnce? Provide the TPR in each part of systemic circualtion
```
total resistance throughout entire system systemic circualtion
50% TPR-> arterioles
20%TPR -> aorta and arteries
20%-> capilalries
10% TPR-> veins
```
113
What is the pressure and resistance throughout pulmonary circualtion? Provide the pressure in pulmonary circualtion in mmHG
- low pressure and low resistance circuit
- approx pressure in pulmonary circulation (mmHg)
Pulmonary artery=15
Pulmonary capillaries = 8
Left atrium = 5
114
why is there huge change in systemic and pulmonary circualtion?
leftvent wall thickness much less than right vent wall thickness- so it doesnt generate as much force
115
Why does the pressure in heart fluculate a lot?
Heart is contraction so as it contracts, it ejects the stroke volume out into aorta and large arteries so the pressure goes up (high pressure = systolic)
- when pressure drops = diastolic pressure (ventricle relax
116
Why is there less ressitance with arteries than arterioles?
They are very compliant (thin elastic walls so that when the blood is ejected out, they could expand to accomodate the stroke volume
- arterioles are very small diameter and not compliant at all, due to the thick walls made of smooth muscle
117
What is systolic pressure
pressure at height of a pulse is 120mmHg, this is when heart contracts, pushing blood out
118
What is diastolic pressure
lowest point of pulse is 80 mmHg, this is when heart is relaxing
119
What is pulse pressure and give the equation
Pulse pressure is the difference between systolic and diastolic pressure
Pulse pressure = systolic pressure - diastolic pressure = 120-80=40mmHg
120
What are the two major factors that the pulse pressure is influenced by?
1. Stroke volume- volume of blood pumped by one ventricle in one contraction; the greater the stroke volume, the greater the rise and fall during systole and diastole, thus causing a greater pulse pressure
2. Compliance- stretchability of blood vessel in the arterial system
- the greater the complance of the arterial system, the less will the rise in pressure for a given stroke volume of blood pumped into the arteries
- because the aorta and arteries stretch to accomodate the rushing in-flow of blood, the greater the compliance, the more stretchable in arterial system
121
Why does aorta have the highest compliance?
- due to the relatively greater prop of elastic fibers vs non-stretchable smooth muscle and collage
- dampens the pressure output of left ventricle thereby reducing pulse pressure
122
What is the windkessel effect?
as blood is ejected into aorta, the walls of aorta expand to accomodate the increase in blood volume.
- if aorta becomes stiff, pressure would be high
123
What is mean arterial pressure
- average pressure throughout the entire system
- slightly less than the value halfway between systolic and diastolic pressure since duration of systole is shorter than diastole
124
What is the equations for the MAP?
MAP=diastolic pressure + 1/3 pulse pressure
= diastolic pressure + 1/3(systolic pressure - diastolic pressure)
= 80+ 1/3(120-80)
= 93mmHg at rest ; can increase when exercising
MAP= cardiac output * total peripheral ressitance
CO- amoutn of blood pumped by heart/min
TPR- total resistance in systol circualtion
125
What is rate pressure product
- way to measure the workload on heart
126
How can you calculate the Rate pressure product
RPP = systolic pressure * HR
units = mmHg BPM
- estimation of how hard the heart is working
- if heart is working hard, the force of contraction and resulting systolic pressure will be increased
127
Flow through blood vessel depends on what two factors?
1. pressure difference between two ends of vessels (pressure gradient) which drives the blodo through vessel
2. the force opposing flow (resistance)
- blood flows from highest pressure to low pressure
- blood flow is decreased by resistance encountered by blood
128
How is the blood flow calcualted by?
```
Q = (P1-P2)/R
Q- blood flow
P1- high pressure
P2- low pressure
R- resistance
```
129
Give the formula for resistance
R= 8Ln/pir^4
l- length of vessel
n- viscosity of fluid
r- radius of vessel
- prop to the length of the vessel and the viscosity of fluid
- inversely prop to 4th power of radius
- small vessel like arteriole despite their short length can offer high ressitance
130
what happens when vessel constrict by 1/2 of its original radius in a blood vessel
- if vessel contstricts by 1/2 of its original radius, resistance can increase 16
131
What is prime in determining resistance
Radius
132
What is the poiseuille-hangen formula and what are the assumptions
Flow = Q = deltaPpir^4/8nl
Assumptions:
1. the tube must be straight, rigid, and cylindrical and unbranched and have a constant radius
2. flow must be steady
133
What are the characteristics of the poiseuille-Hangen formula. ie. What is flow directly and indirectly prop to?
Flow is directly prop to pressure gradient, and the 4th power of vessel radius
The flow is inversely prop to both the elngth of vessel and viscosity of fluid
134
What is the simplified equation of blood flow: and what do you assume?
Flow = Q= delta P * r^4
- viscosity of the blood doesnt change
- length of blood vessel doesnt change
135
Describe the simplified blood flow
- small changes in radius has a more dramatic effect on blood flow than change in pressure
a. the amount of blood flow to individaul vascular beds can becontrolled separately (vasodilating/constricting)
b. there is relatively low resistance to flow
- lowers the pressure requirement for blood flow
- decreases work load on heart
136
Why do you have parallel circuits
- there is shorter length in parallel circuits, which reduces the resistance
- bloow flow to individual vascular beds can be regualted vasomotion -> either vasodialting (increasing blood flow) or vasoconstricting (decreasing blood flow)
137
How do tissues regulate blood flow?
Intrinsic- built into tissues to allow tissues to regulate its own blood flow
Hormonal- circulating chemicals such as hormones and neural mechanisms dealing with autonomic nervous system
138
What the structure of walls of blood vessel?
It contains 3 layers:
1. Inner tunica interna- predominantly endothelial cells
2. Middle tunica media- contains curculaly arranged elastic tissue and vascular smooth muscle (vary which part of arteriole system your looking at)
3. Outer tunica externa- entirely connective tissue fibrous
Capillary has only one layer of cells- endothelial celsl
Veins- have valves becasue BP is very low on venous side of circulation so this ensures that blood travels in one direction
139
Draw the structure diagram of blood vessel structure
See E. Cardio
140
How does aorta vessels structure relate to the function?
- thin walls with inner layer made of elastic tissue
- blood is ejected into aorta as it expands
- can accomodate rush of blood (pulsatile nature)
- pulse pressure is strongly influenced by stroke volume and compliance (elasticity of blood vessel)
- maintian increase blood pressure to distribute throughout the body
141
How does the arteriole structure related to its function?
- lots of smooth muscles - thick wall
- good at regulating blood flow to various tissues
- blood flow depends on pressure gradient that drives blood from one end to other and also affected by radius of the vessel
- drop in BP is directly related to resistance it encocunters as it moves through
- highest in resistance and drop in blood pressure
- under autonomic control- dilate/constrict them
- thicker than aorta
142
How does the capillary structure relate to its function?
- one cell thick
- highest cross sectional area
- suited for exchange of substances
- short diffusion distancce
- low velocity, high cross-area, short distance -> gas exchange
143
How does the vena cava structure relate to its function?
- large diameter and thinnerr wall compared to aorta
144
How ddoes the structure of vein compare to its function?
- low BP
- large diameter
- lots of smooth muscle content in walls
- thin walls
- can accommodate predominantly most of our blood
- when they constrict = increase venous return = increase EDV = Increase SV
145
What is the purposes for cardiovascular mechanism? Name 4
Homeostasis
- increase blood supply to active tissue
- increase or decrease heat loss from the body by redistributing blood
- maintain blood supply to vita organs - the heart and brain- at all times
- maintain blood pressure (mean arterial pressure)
```
High resistance = High BP
No proper blood flow = BP too low
MAPS= driving force of blood through circulatory system
MAPS= CO * TPR
CO= HR * SV
```
146
What are the mechanism for the control of circulation grouped into three types? ie CV regualtory mechanism control
a. local control mechanism (autoregulation)- by tissue itself
b. hormonal regulaation (substances in blood)
c. neural control mechanism of blood flow control (ANS)
147
What is the local control mechanism for autoregulation?
Autoregulation- most tissues have the capacity to control their own blood flow
- process by which individual beds maintian a relatively constant blood flow when changes occur in pressure
- blood pressure varies within certain limits (50-150 mmHg)
- local mechanisms will be involved to maintian a realtively constant blood flow
blood flow is directly prop to pressure gradient
- when blood vessel constrict, the pressure increase upstream and decreases downstream
148
What are the two theories to explain autoregulation?
Myogenic theory - muscle and metabolic theory- metabolites in blood
149
Explain the theory of myogenic theory
How arteriole react to an increase or decreasae in BP
- when BP inccrease, the artiole will initially dialate
- this leads to a reflex constriction to maintain BP and flow
- has protective effect so delicate capillaries are not damaged
BP increase leads to constriction of blood vessel
1. increase arterial pressure distends blood vessel (Arteriole); no AP is necessary, the level of entered Ca affects level of constriction proportionally
2, stretch of vascular smooth muscle (VSM)
3. opening stretch activated ion channel
4. depolarization of cell memrbane which causes calcium entery via VG calcium cahnnels
5. constriction of VSM
6. vasoconstriction = increase resistance to blood flow due to decrease pressure downstream
* if arterial pressure decrase, there is less stretch of VSM, the vessel remain relatively dialated, preventing decrease in blood flow
150
Draw the diagram to explain Myogenic theory
Autoregulation occurs as a result of locally induced vasomotion (vasodilation/constriction) due to diret sensitivity of resistance vessel (arterioles) to pressure within lumen
- protective effects so delicate capillaries are not damaged due to sudden increase in BP
* * arterioles constrict to pretect capillaries from huge surge of load
- after baylis effect, the blood flow returns back to normal if pressure drops
151
What is the metabolic theory
- autoregulation occurs as a reuslt of locally induced vasomotion due to presence/absence of vasodilatory metabolities VDM in region of arterioles
152
What are the VDMs?`
a. decrease O2- metabolically active tissues (tissues will start to use oxygen)
b. increase H+
c. increase CO2
d. inccrease temp
e. increase K+ extracellular cause vasodilation in active tissue
f. increase lactic acid
g. increase adenosine - from ATP breakdown
* in kidney where adenosine will constrict afferent artiole which is what we want during exercise (decrease blood flow to kidney)
153
What is the mechanism by which tissues regulate blood pressure due to metabolic theory
1. increase arterial pressure
2. increase blood flow initially
3. VDMS washed away
4. Vessel constricts
5. inccrease resistance to blood flow
6. flow reduced to normal
- if arterial pressure falls initially, flow iwll be reduced causing accumulation of VDM resulting in vasodialtion and increase BF
154
What is reactive hyperthermia
- increase in blood flwo resulting from brief period of occulusion- allows buildup of VDM andd depletion of oxygen
- once occulusion is remove,d tand the blood flow is restored, there is a transient inccrease in BF becasue the blood vessel will be more dialated
155
What happens when you shut off all flow to arm?? how do they tissues deal with this to autoregulate?
- tissue still metabolically active- VDM build up
- happens after removing a tourniquet or blood pressure
- get sudden surge in blood flow, eventually that increase BF will wash all the metabolites
156
What happens during active hyperthermia?
During exercise:
1. increase in blood flow
2. increase in production of VDM
- 3.vessel dialate
4. increase blood flow to acive tissues
- increase in VDM in metabotically active tissue - decrease O2, increse Co2, lactic acid)
157
When you are exercising, what theory is a stronge regulator of active tissue?
when cycling, want most of the blood to go to your legs, cardiac output is increased
- tissues regulate its own bloodd flwo by secreting all these vasodialtor metabolities to dialte all the vessels ,so a lto of blodo flwo goees to active tissues
THe metabolic theory is strongest regualtor of bloow flwo to active tissue during exercise?
158
Explain why when you hyperventilate for a long time, you will pass out
Hyperventitlate- break very fast, decrease COC2
- leads to narrowing of blood vessel that supply blood to brain
- leads to bain depleted of oxygen- passing out
159
What is hormonal regulation?
- regulation by substances present in blood
- control blood flwo and maintain blood pressure by producing changes in vascular resistance
- achieved with vasoconstrict agents and vasodilator agents
160
What are vasoconstriction agents and what are the 4 types?
Vasoconstrictor are substances that constrit the blood vessel
- decrease blood flow, incrrease MAPS by decreasing diameter and inccreasae TPR
Substances:
1. Epi/Norepi
2. AngioTension 2
3. vasopressin
4. endothelin
161
Is epi/norepi vasoconstriction or vasodilation agent and how does it accomplish it?
Vasoconstriction
- sected by adrenal medulla bby SNS in msot vascular beds
- binding to alpha 1 adrenergic receptors
- cases vasoconstriction in most vascular beds
162
Where are alpha, beta 1 and beta 2 adrenergic receptors located? WHat effect do they cause?
alpha - located on the arteries
- stimulated by epi or neoepi, they constrict
- increases blood pressure and blood flow returning to the heart
- blood essel in skeletal muscle lack alphaa receptors becasuse they need to stay open to utilize increase blood pumped by the heart
Beta1- located in heart
- increase heart rate and increase hearts strenth of ocntraction
beta 2- located in bronchioles of lungs and arteries of skeletal muscles
- when the receptors are stimulated, they increase diameter of bronchioles to let more air in during breathign and they dialate the vesse of skeleta muscle so they can receive the increased blood flow
163
What happens when you adminster epi, we exect alpha, beta 1 and beta 2 agonist effects such as
- increasae BP
- increae HR
- increased cardiac contractile
- dialate bronchioles in lungs
- dilate vessels in skeletal muscle
164
What are the two types of parasympathetic receptors?
Muscarinic and nicotinic receptors
Nicotine- muscle contraction
Muscarinic- causes decrease in heart rate, heart contractility and ecreasae in size of bronchioles
165
Is Angiotensin a vasoconstriction or vasodilation agent and how does it accomplish it?
Vasoconstriting
- powerful and most potent formin in body
- production is stimulated by a drop in bloodp ressue and a drop in Na levels
causes an increase in arterial pressue (MAPS)
Angiotension (mainly from liver - (decrease BP, Na -> renin released fro kidney) --> ANg1 -- (Angiotensin converting enzyme (ACE, found in lungs) --> Ang2- MAp increased
Other effects:
- peripheral vasoconstriction, which will cause increase arterial pressure
- increase synthesis and secretion of NE at sympathetic nerve ending which will casue an increae in arterial pressure
166
Is Vasopressin a vasoconstriction or vasodilation agent and how does it accomplish it?
vasoconstrictor
- also called antidiuretic hormone
- fomred in hypothalamus and released by posteror pituitary
- promote water reabsorption in remal collecting tubule
- increase conc of ADH appears in blood following
hemorrage-> produces vasoconstriction and will increase MAPS
167
Is Endothelin a vasoconstriction or vasodilation agent and how does it accomplish it?
- present in endothelium of most blood vessel
- released by damaged blodo vessel, such as crushing itssues
- proteins found in endothelial celsl are most blood vessels (inner layero f blood vessse, since endothelial cells form the inner layer of blood vessel
168
Is Epi a vasoconstriction or vasodilation agent and how does it accomplish it?
Vasodilation
- mild vasodilation in skeletal and cardiac muscle and liver
- binds to B2 adrenergic receptor causing smooth msucle to relax leading to vasodialtion
- norepi doesnt bidn to b2 adrenergic receptors
169
Is bradykinina vasoconstriction or vasodilation agent and how does it accomplish it?
- formed in blood or body fluids
| - histamine (released by every tissue when its damaged proabbly derived from eosinophils and msut cells
170
Is Nitric oxidea vasoconstriction or vasodilation agent and how does it accomplish it?
- endothelial relaxing factor
- potent vasodialtor
- released by endothelial and causes relaxation of smooth msucels in walls of bloodd vessel causign vasodilation
- No binds to receptrs on vascular smooth msucle - increase cGMp and cGMP ledas to relaxation by increasing vessel radius and causes inrease in blood flow into tissues
Nitroglycerine used to treate chest pain which is converted to NO in body
- viagra presents breakdown of cGMp, increase blood flow
171
Is prostaglandinsa vasoconstriction or vasodilation agent and how does it accomplish it?
- produced lcoally from endothelial cells
| - relaxation of smooth msucles to produce vasodialtion
172
Is Atrial natriuretic factor a vasoconstriction or vasodilation agent and how does it accomplish it?
- produced by atrial muscle cells- powerful
- released from atrial musclce cells when atrium is stretched
- caused by increase in blood volume
173
What is the mechanism of epi in stumlating sympathetic
- increase HR, FOC, divert blood and oxygen to areas that need it
- release EPi - binds alpha -> constriction
- bidns beta - dialtion (skeletal, cardiac and liver
ALPHA CONSTRICTS AND BETA2 DILATES
174
How can the ANS cause neural control mechanism?
- causes rapid changes to blood vessel diameter resulting in vasoconstriction/vasodilation
- Recall: change in vessel diameter (radius) will cause change in peripheral resistancce
R = 1/r^4 - regualtes bloodd flow to organs in fight/flight and rest nd digest situations
175
Describe the mechanism by whcih SNS and PNS causes neural control mechanism
1. SNS vasoconstrictor- release norepi onto blood vessel, bind to alpha adrenergic receptor to constrict
- causes increase in resistancce and decreae in blood flow below the constrcition
2. Sympathetic cholinergic vasodilator fibers- activated in humans in extreme fight and flight resposne
- most skeletal muscel release ach- produce vasoconstriction - increase blood flow to musclces
3. PNS doees not directly affect blood vessel diameter
- when PNS is activated, SNS is shut off
- SNS off
- > removes its constricting effects on blood vessel and resilts in vasodialtion and increase blood flow to vessel
176
What is the ANS neural control and what is its purpose?
neural control mechanism invovles rapid adjustment to cardiac output and total peripheral ressistance
- purpose is to maintian normal mean arterial pressure for proper perfusion of tissues throughotu the body
MAP = CO * TPR
177
What is the effect of vasoconstriction and vasodialtion on TPR?
Vasoconstriction will increase TPR and Vasodilation will decrease TPR
178
ANS
- control short-term homeostatic mechanism
- imputs that stimular/depress activity in autonomic nerves
- >reflec pathways
- > inputs from CNS tha trigger responses to stress, emotions and exercise
179
How can you maintain mean arterial pressure?What two factors would influence MAP and how?
- by regulating cardiac output (flow of water out of tap) and TPR (kink in the hose)
Turn flow down - decreasae CO, decrease MAP flow out of the heart decreases, than you will decrease the pressure and vice versa
Kink in Hose
- decrease radius, inccrease resistance, increase MAP
vice versa
MAPS = CO * TPR
180
How does the cholinergic and adrenergic system deal with mean arterial rpessure?
Cholinergic system will decrease the arterieal pressure by release of Ach
Adrenergic system ill increase in arterial pressure by dealing with reelase of NorE
181
How can you control MAPS by cholinergic control? Write the two mechanisms
1. Stimualte the parasympathetic fiber to heart
2. relase Ach; binds to muscuranic receptors on SA and AV node
3. decrease HR and force of contraction - Ach decrease slope of pre-potential which will decrease HR an FOC
4. decrease CO and decrease MAPS
- > change maps by changing only CO
1. stimulation of sympathetic cholinergic vasodilator fibers to peripheral tissues (skeletal muscles)
2. reelase Ach
3. Dilation of blood vessel (arteriole) in skeletal muscles
4. decrease peripheral resistancec
5. decrease MAP - would decrease if no other mechanism were occuring
During exercise, many changest including increase HR and SV which will increase MAP
- this mechanism is only seen in extreme fight/flight response
182
How can you control MAPS by adrenergic control?
1. Stimulation of symp fibers to heart
2. release norepi; binds to beta 1 receptors; will increase slipe of prepotential; binds B1 receptors on cardiac contractile cells = increase calcium entering the cell = increase contraction
3. increase HR and contractile force
4. increase cardiac output
5. increase MAP
1. stimualtion of symp nerve to adrenal medulla
2. release acetylcholine onto adrenal medulla
3. secretion of epi 80% and norepi 20% into circulation binds to beta 1 receptors in heart
4. increase HR and contractile forcce
5. Increase cardiac output
6. increase MAPS
1. stimulation of symp vasoconstrictor fiber to most peripheral blood vessel
2. Norepi reelased which acts on alpha adrenergic - doesnt bind to b2
3. vasoconstriction
4 increase TPR
5 increase MAPS
183
Describe the overall ANS control of blood flow , epi and norepi during fight and flight response
- symp post gang noradrenergic fiber reelase nrepi which bind to alphaa adrenergic receptor to cause vasoconstriction
- norepi doesnt bind B2 receptors so doesnt directly cause vasodialtion
B1 receptor in heart increase HR which are diff from B2 receptor in blood vessel
- to cause vasoconstriction, remove the symp activation of these fibers- reducting the symp activity will cause decrease in norepi and its vasoconstricting abilit ywhich will cause vasodialtion
- constricting effects of neoepi blocked by pesence of vasodialtor metabolities, prodced by active tissue
- SNS causes vasoconstriction by binding alpha receptors- even in skeletal muscles, if the muscle becomes active, and prodces VDM, the VDM will block constricting effects of neorpi, directly causing local vasodialtion through metabolic theory of blood flow regulation
SNS causes release of Norepi from psot gang sym fiber and at the same time, causes release of Ach from symp cholinergic vasodialtory fieber- effect weak in humans compared to norepi -> overall vasoconstriction
Epi from adrenal gland can bind
1. alpha receptor- cause vasoconstriction - found throughout body , more alpha receptors than beta receptors
2. beta 2 receptors - vasodialtion of blood vessel- found in skeletal muscles, cardiac andd liver
- when epi released from adrenal gland, it will vasoconstrict blood vessel throughout body where blood isnt needed and direct it to places needed vasodilation in skeletal muscels- during fight and flgith
alpha constrict and beta dilates
184
List the overview of mechanism for control of circulation:
1. local mechanisms
- myogenic theory
- metabolic theory
2. humoral mechanisms
- vasoconstrictor (increase MAP)
- vasodialtors (Decrease MAPS)
3. neural mechanism (ANS)
- cholinergic - decrease MAP
- adrenergic increase MAP
185
What is the baroreceptor reflex?
- homeostatic mechanism - negative feedback
- maintain normal mean arterial pressure for proper perfusion of tissues throughout the body
- invovles rapid adjustment to both cardiac output and total peripheral resistance
MAPS = CO * TPR
186
WHat are the two specialized structures that baroreceptor eflex relies on?
1. mechanoreceptors - high pressure baroreceptors and low pressure volume receptors (not involved in baroreceptor reflex)
2. CV control center in medulla
187
Where are the high pressure baroreceptors located and what are they for?
- located in walls (tunica externa) of aortic arch and carotid sinus
- stretch sensitive receptors constantly monitor changes in arterial pressure and reply info to CV center
- increased BP -> stretches walls of blood vessels -> increase AP firing rate by the baroreceptors - signals sent to CV center
- monitor changes in blood pressure and relay info to cardiovascualr center in the brainstem to adjust CO and TPR
188
Where are the low pressure volume receptors located? and what is their role?
not invovled in baaroreceptor reflex
- located in left and right artium
- free nerve ending detect fullness of circulation
- help regualte blodo volume
- Blood pressure is related to blood volume :
the higher the blood volume -> the higher the MAP
189
What does a drop in blood volume (Drop in Map) cause?
| What does an increasae in blood volume (increase in MAP cause)
- when your dehydrated, there is a drop in blood volume
- release ADH - help retain water and causes vasoconstriction in high conc
- renin release -> formation of Ang2 vasoconstrictor
- Ang 2 also stimulates third
increase in blood volume will
- decreasae in ADH, renin and Ang 2
- increase atrial natriuretic factor - hormoral vasodilator
190
Draw a diagram of the baroreceptor reflex
See lecture 10 Cardio
191
Describe the baroreceptor reflec mechanism
- high pressure baroreceptors send singals (afferents from baroreceptors) in cardiovascular center to medulla through Vagust nerve (from aortic baroreceptors) and carotid sinus nerves ( from carotid sinus baroreceptors)
- CV is going to compare the input the set point and send singals output
192
What is the output from Medulla Baroreceptor reflex? PNS and SNS
PNS efferent fiber vagus nerve will send signals to the SA and AV node and tiny little singal to cardiovascular contractile cells to release Ach and decrease the heart rate and contractile force
SNS efferen fiber will travel down to spinal cord, exit the spinal and pre gang will synapase in symp gang that will either travel to the
1. - NE release; heart to intervate the SA, AV and cardiac contractile cells to increase HR and force or contraciton
2. arterials and veins by release NE to bind to alpha 1 causing them to constrict
193
Wht is the CV center in brain and name the main components
CV center is located in medulla of the brain stem
Main components include:
a. the solitary tract nucleus (NTS)- receives all the info from baroreceptors
b. vagal center (cardio-inhibitory area) - nerve info originates
c. Vasomotor center
194
Draw the diagram of the baroreceptor reflex CV center?
- all info comes in brainstem and synapse in solitary tract nucleus
- excitatory interneuron from solitary tract nucleus and vagal center (cardio-inhibitory area)
- signals will cause excitaton of the vagal center
- Inhibitory interneuron between Solitary tract nucleus and vasomotor center
- singal will shut of the vasomotor center
195
What happens when solitary tract nucleus in medulla of baroreceptor reflec is shut off?
- there would be no excitatory input to vagal center, which will shut it off
- there would be no inhibitory input to vasomotor center, which will keep the vasomotor center on
Vagal center - sends vagal nerve to heart to release Ach as PNS
Vasomotor center wil lsynapse on SPinal Cord and release NE to incrrease HR and force of contraction
196
What is the response of High BP in carotid and aortic baroreceptors?
1. stimulated by stretch (increase BP)
2. increased AP generation
3. Increase AP traffic to solitary tract nucleus : 2 ways
a1. activation of vagal center
a2. vagal traffic t o heart
a3. Ach released
a4. decrease HR, decrease CO and decrease BP
b1. activation of inhibitory interneuron to vasomotor center
b2. decreased sympathetic outflow to Heart and bloow
b3. HR decrease, CF decrease and dilation occurs
b4. Decreae CO and decreasae Ressitance
b5. BP decrease
197
What happens in response to high BP?
1. Carotid and aortic baroreceptors
2. decreaased stretch
3. decrease AP generation
a. decreased activation of vagal center
a2. decreased vagal traffic to heart
a3. no Ach released
a4. HR increasaed, CO increased and BP increased
b1. no activation of inhibitory iinterneuron to vasomotor center
b2. increasaed sympathetic outflow to heart and blood vessel
b3. increase HR, CF and constriction
b4. CO increased and resistanace increased
b5. BP increased
198
How can you regulate CV during emotional stress?
1. increase activity of symp cho vasodialator diber to muscle arteriole- dialtion
2. increase activity of cho fiber to sweat glans- sweating
3. increase activity of symp fiber that release Ach on to adrenal medulla to release epi which dilates muscel arteriole and constricts kidney, intestine arteriole - increase HR and SV
4. decrease activity of vagal nerve (reelase Ach) and increase activity of symp post gang fiber NOR to heart (increase heart rate and contractility)
5. increase symp outflow to veins (capacitance vessels) constriction - increase EDV
6. increase symp outflow to the renal and splanchnic (intestine) resistnce vessel- constriction
199
What are the four mechanism of CV regulation during exercise?
1. Local
2. mechanism
3. Nervous system
4. Hormonal
200
What is the local mechanism of CV regulation during exercise?
- arterioles dialte in active muscles due to vasodialtor metabolites (VDM)
- a very powerful mechanism
- VDM also block the symp vasoconstrictior effect on the msucel vessel (SNS trying to vasoconstrict blood vesel via Norepi)
201
What is the mechanical CV regulation during exercise?
- during dynamic exercise, the muscle pump retrns blood from lower limb to the central circulation - increase venous return, increase EDV, increase SV, increase CO and increase MAP
202
What is the CV regulation via nervous system during exercise?
- increase symp outflow to the heart and systemic blood vessels
- decrease vagal outflow to the heart decreases
- tachycardia- incrrease HR
- increase Cardiac contractility, increase CO and increase MAPS
- constriction of resistance vessels in kidney and intensitne and splanchnic veins
As exercise continues, and the body temp begins to increase, the temp sensitive celsl in hypothalamus are activated
- inhibit the symp outflow to the skin vessels and stimulate the cholingergic fibers to sweat glands
- this results in dilation of skin vessels and sweating
203
What is the hormonal CV regulation during exercise?
- If exercise is intense, the cholingergic fibers to the adrenal medulla are activated and epi is released into blood stream
- enhances the heart rate and contractility, constricts veins and arterioles and dilates blood vessels in skeletal muscles (AC/BD)
