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Physiology 210 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

functions of the cardiovascular system

A
  • bringing nutrient into the body (e.g. from the intestine to liver)
  • bring fuel to cells
  • bringing O2 to cells from lungs
  • removal of waste products
  • circulation of hormones
  • circulation of immune cells and antibodies
  • regulation of electrolytes
  • regulation of pH
  • H2O balance
  • thermoregulation
  • …….transport, transport, transport
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2
Q

Does an amoeba need blood

A

No

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3
Q

Fish Circulatory System

A
  • Closed circulation
  • Single loop circulation
  • 2 chambers
  • has gill capillaries + systemic capillaries
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4
Q

Amphibian & Reptilian Circulatory System

A
  • 3 chambers
  • double-loop circulation
  • closed circulation
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5
Q

Mammalian Circulatory system

A
  • 4 chamber heart
    -double-loop circulation
    -closed circulation
    Right side
    -pulmonary circulation
    Left side
    -Systemic Circulation
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6
Q

Septum

A

Part of the heart that separates the two sides

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7
Q

Haemodynamics

A
  • the branch of physioology dealing with the forces involved in the circulation of the blood
  • the circulation and movement of blood in the body and the forces involved therein
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8
Q

Volume (blood)

A
  • 75% of weight is blood (75 kg man)
  • 60% of blood is in the veins, why venous system is called capacitance
  • Arterial system is called resistance, less blood flowing
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9
Q

Flow (blood)

A
  • purpose of the card. system is to create flow
  • flow coming into the heart has to be equal to flow coming out of the heart
  • Flow = Volume/Time
  • Flow = area x (mean)velocity

Flow = perfusion pressure/resistance

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10
Q

Flow from the left Heart

A

Cardiac Output

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11
Q

Flow from the right heart

A

Venous return

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12
Q

Total Cross Sectional Area and Flow Velocity

A
  • Total cross section area increases as you go closer to the capillaries
  • crs. sct. area decreases as you go towards the vena cava from the capillaries.
  • Crs. Sct. area determines the pressure of the flow.
  • Low flow velocity allows a more efficient transfer of oxygen
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13
Q

Pressure (blood)

A

-Pressure = Force/Area
S.I. unit: pascal(Pa) = newton/m^2
-n.m. 120/80 mmHg

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14
Q

Hydrostatic Pressure

A 
Volume = area x height 
Mass = density x volume
F= mass x acceleration due to gravity
Pressure = Force/Area
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15
Q

Perfusion Pressure

A

Perfusion pressure = inlet pressure - outlet pressure
- The thing that will drive the flow is the difference between pressure

= arterial pressure - venous pressure

P = Pa - Pv

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16
Q

Resistance (blood)

A

Resistance = Perfusion pressure/ flow

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17
Q

Laminar or Parabolic Flow

A
  • Smooth flow: lamiar or parabolic flow
  • near the wall velocity decreases
  • highest velocity is at the midline of the vessel
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18
Q

Friction losses in a viscous flow

A

generation of heat –> fall in pressure down the vessel.

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19
Q

Control of vessel resistance

A
  • Vessels can contract or relax

- This changes the radius, thus affecting the flow of blood

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20
Q

Vessels in Series

A

Resistance = R1 + R2

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21
Q

Vessels in Parrallel

A

1/R = 1/R1 + 1/R2

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22
Q

Cardiac Valves

A
  • all of the valves sit in the fibrous ring (connective tissue)
  • bicuspid = two leaflets
  • tricuspid = three leaflets
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23
Q

Injection Phase of the Heart

A

Ventricle contraction –> pulmonary valve opens –> valve then closes because the pressure in the ventricle falls as the heart stops its contraction process, at this point the pressure in the pulmonary track will be higher.

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24
Q

Chordae Tendinae

A

little fibers that attach the muscle to the cardiac valves

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25
Q

Sino Atrial (SA) Node

A

pacemaker of the heart. Activates a small amount of cells.

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26
Q

Endocaridium (enothelium)

A

muscle on the inside of the heart, closest to the blood

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27
Q

Epicardium

A

muscle just outside of the heart, second

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28
Q

Activation Sequence of the Heart

A
  • need contraction of the atrium then the ventrile
  • SA node sends signal that depolarizes the cells, sending electrical signals through the right atrium. The wave will die at the fibrous ring but will contrinue through the AV node –> then enter the bundle of HIS –> break into two bundles –> keep breaking up into very fine fibers –> purkinje fibers.
  • These fine fibers tend to be in the endocardial muscle in the ventricle (NOT IN THE EPICARDIAL MUSCLE).
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29
Q

Muscle that first gets activated

A

Endocardial muscle then to the epicardial muscle, This creates a contraction.

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30
Q

Intercalated Disc

A

-Dark lines between cells

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31
Q

Nexus or Gap Junction

A
  • as you go along the intercalated disc, you will run into a gap junction.
  • Nexus = a connection or series of connections linking two or more things.
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32
Q

Hemi-channel or Connexon

A
  • Channels that connect two cells
  • If the membranes are close enough they will dock
  • Through these channels, action potential can travel.
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33
Q

Local Circuit Currents

A
  • Cells usually sit at -90mv
  • Action potential is moving left to right
  • Resting cell is negative compared to the outside
  • Activated cell –> +40mv
  • Potassium ion will move into resting cell due to opposite charge attraction
  • Sodium ion will move into newly activated cell from unactivated
  • Negative charges leave about to be charged cell
  • Need both intra and extra-cellular flow
  • Causes depolarization across the membrane
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34
Q

ECG Waves and Complexes

A
  • P wave
  • Q wave
  • QRS complex
  • R wave
  • T wave
  • amplitude ~1mV (vs 100 mV for an intracellular recording)
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35
Q

P wave

A

-indicates activation of both atrium. Only until the AV node do you see the Pwave

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36
Q

QRS complex

A

Activation of ventricles
Q –> Atrial Relaxation
RS –> Activation of the ventricles propagation

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37
Q

T wave

A

-repolarization from the ventricular muscles. (ventricular relaxation)

38
Q

Ionic Basis Underlying Ventricular AP

A
  • At rest, permeability to K is relatively high, permeability to sodium and calcium are low.
  • When a membrane is only permeable to K it will reach close to -100mV.
  • This is why at the start the membrane is close to -100mV
  • The local currents is what causes the initial spike in potential
  • Action potential will change the permeability to Na
  • The positive Na ions will be attracted to the negative charge on the inside of the cell. Influx of Na ions.
  • There is also a higher conc. gradient of Na outside the cell forcing ions in.
  • Both conc. force and electrical force, will force ions into the cell
  • This will depolarize the cell
  • Fast inward Na current = quick turning off and on of Na Channels
39
Q

Ionic Basis Underlying Ventricular Ap continued

A
  • One class of K channel closes as result of depolarization –> permeability of K decreases
  • Ca channels will notice increase in voltage, Ca channels activate slowly
  • Ca channels are slow to open and close
  • Conc. of Ca outside the cell is very high –> high force to push Ca ions into the cell
Another class of K channels that are lazy will wait till the end after recognizing the voltage increase, to open
-This causes the cell to repolarize (more negative)
40
Q

SA node Action Potential

A
  • Instead of going back to resting potential after firing, it slowly depolarizes
  • will slowly hit the threshold and fire
  • no resting membrane potential in the Sinus node
  • Here the influx of Calcium is what causes the depolarization
41
Q

Purpose to why conduction velocity in the AV node is slow

A

the atrium needs to finish contracting before the ventricle begins contracting. Hence delay between the contraction of ventricle and atrium.

42
Q

Sinus Bradycardia

A

rate

43
Q

Sinus Tachycardia

A

rate > 100/min

44
Q

Sinus arrhythmia

A
  • on inspiration rate goes up

- on expiration, rate goes down

45
Q

2:1 Atrioventricular Block

A
  • Two p waves for one QRS and T
  • P wave gets blocked somewhere in the AV, bundle of his or further down.
  • Problem is that the ratio of P wave blocks may increase causes of failure of ventricle contraction
  • Treatment: place an electronic pace maker in the heart.
46
Q

Complete Atrioventricular Block

A
  • P wave gets blocked somewhere in the heart.
  • No QRST at all
  • Treatment: “odds are you put in a pacemaker”
47
Q

What happens in the ventricles during a complete atrioventricular block

A
  • somewhere in the ventricles there is an area that has become a pacemaker
  • spontaneously creating action potentials (thought to be in the purkinje fibers)
  • SA node and atria are working together, whilst the ventricles are working at their own rate.
48
Q

Premature Ventricular Contraction

A
  • Ectopic beat because it comes from an ectopic pacemaker

- Ectopic means it is in the wrong place

49
Q

Ventricular Tachycardia and Fibrillation

A
  • Heart pumps sporadically, ventricles pump out blood, atria do no not pump blood into ventricles. Blood does not circulate body
  • can be caused by a pre ventricular contraction (PVC)
50
Q

Top of the heart is known as

A

the base

51
Q

Bottom of the heart is know as

A

the apex

52
Q

Left side of the heart

A

epicardial sack

53
Q

Circus movement reentry

A

Action potential keeps traveling around the heart non-stop. Purkinje fibers must going into the atrium, or there is some sort of connection.

54
Q

Pulmonary Vein Isolation For treatment of atrial Fibrillation

A
  • cells are frozen to stop propagation of premature stimulus.
  • when the action potential is released it would die in the ring of dead cells created.
55
Q

Excitation-Contraction Coupling

A
  • Action potential will run down the membrane
  • The increase in voltage will be noticed by the Ca channes
  • Ca will flood into the cell
  • Ca that gets into the cell will bind to a receptor(ryanodine receptor) on the sarcoplasmic Reticulum
  • SR is fucll of Ca at high concentration
  • Ca that leaves the SR and goes into the cytoplasm
  • The Ca will then combine with the troponin on the actin (in muscle)
  • Thus resulting in contraction

*there is a Ca pump that keeps the SR concentration high

56
Q

Pulseless electrical activity

A

action potentials are being sent off but no mechanical activity or pulse

57
Q

Systole

A

-Ventricles start to contract –> atria ventricle valve opens –> the ventricle does not need to contract for very long until the pressure inside exceeds the pressure in the atrium –> atrial valves close.

  • Systole refers to the fact that the ventricle is contracting
  • At some point the pressure in the ventricle exceeds the pressure in the aorta –> the aortic and pulmoary valves open and blood is ejected.
  • The ventricle is still contracting, the pressure is still going up

-The ventricle will then relax and the pressure drops.

58
Q

Isovolumetric Ventricular Contraction

A

the blood volume is fixed, ventricle contract, so the pressure inside increases.

59
Q

Diastole

A
  • Filling of the heart
  • The pressure in the ventricle is less than that of the aorta and pulmonary arteries –> the upper valves close –> the volume inside the ventricles is fixed –> enter the third phase –> the pressure in the ventricle falls lower than than the atrium.

-Blood enters the ventricle at relaxation and at atrial contraction.

60
Q

Stroke Volume

A

Stroke Volume = End Diastolic Volume - End Systolic Volume

e.g. SV = 120mL - 50mL = 70 mL

61
Q

Ejection Fraction

A

EF = Stroke Volume/ End Diastolic Volume
e.g.
EF = 70mL/120mL = 0.6 (60%)

62
Q

Cardiac Output

A

CO = Heart rate x Stroke Volume

e.g.
CO = 70 per min x 70mL
=4900 mL/min
= 5 L/min

63
Q

End diastolic volume

A

volume when the ventricle is filled

64
Q

End systolic volume

A

volume when the blood is ejected

65
Q

Starlings Law of the Heart (Frank-Starling Mechanism)

A
  • If you increase the filling of the ventricle, then it contracts, the stroke volume will increase.
  • The muscle will contract more forcefully because it is more stretched
  • Stroke volume increases with volume increase.

-Right Atrial pressure is used as an indicator for pre-load

66
Q

Abnormal Valve (Stenotic valve)

A
  • fucked up valve
  • narrowed valve
  • turbulent flow = murmur
67
Q

Abnormal valve (Insufficient valve)

A
  • valve allows backflow of blood
  • leaky valve
  • Turbulent backflow = murmur
68
Q

Total Peripheral Resistance TPR (Systemic Vascular Resistance)

A
  • resistance of all the arteriole, etc.

- TPR = (Blood Pressure Mean (BPM) - Pressure in the right Atrium (Pra) )/ CO

69
Q

Blood Pressure Mean (BP mean)

A

= CO x TPR
or
= HR x SV x TPR
*usually around 100 mmHg

70
Q

Control of Vessel Tone

A
  • Local factors: depending on what organs are around it. (local or metabolic)
  • Neural: all vessels have some type of neural innervation
  • Hormonal : hormones that flow through the blood
  • Vessel tone: state of constriction of the vessel.
71
Q

Pulmonary Vascular Resistance

A
  • this is the resistance of the blood going through the lungs
  • perfusion pressure is 10x smaller in the lungs, but the flow is the same
  • Resistance is smaller than systemic
72
Q

Systemic vs Pulmonary Circulation

A

Systemic Circulation - High Pressure, High Resistance

Pulmonary Circulation- Low pressure, low resistance

*flow is same for both

73
Q

Coronary Arteries

A

-Heart feeds itself first. First arteries that come out of the aorta are the coronary arteries

74
Q

Coronary Autoregulation

A
  • when perfusion pressure decreases, the coronary flow will also decrease.
  • coronary flow will bounce back up via decrease or increase of resistance depending on the state of the Coronary Perfusion Pressure (CPP)
75
Q

Two mechanisms of Autoregulation

A
  1. Metabolic
  2. Myogenic (muscle)
  • When flow of blood decreases, the O2 decreases to the tissue. Increase in waster products
  • Vessel wall stretch decreases
  • Metabolites act on the tissue relaxing it in turn –> decreasing resistance
  • Resistance of the flow decreases –> flow increases
  • Smooth muscle will recognize the fall in stretch –> decrease in resistance.
76
Q

Local Metabolic Control

A

Increase metabolic activity –> decrease in O2 and increase in metabolic waste –> relaxes smooth muscle –> vessel will increase in cross sectional area –> resistance goes down –> flow increases

77
Q

Activate the parasympathetic on Heart

A
  • Slow the rate of the SA node

- ACh binds to receptor on the SA node –> slow it down

78
Q

Activate the sympathetic system on heart

A
  • increase rate of SA node
  • Atropine, drug to get heart rate up. Binds to the muscarinic receptor. Stops ACh from binding which would have lowered the heart rate.
79
Q

Sympathetic Control of Contractility

A
  • Pre ganglionic axon, ACh neurotransmitter to nicotinic receptor. Two post ganglionic axons with NE released on the Sinus node.
  • Send axons to the ventricular cells –> NE makes the cells contract, increase force of cell (increase size of Ca count)
  • B-agonist will bind to Beta receptor and increase the contraction of the cells –> increase stroke volume, increase CO, and BP
  • B-antagonist: block receptor –> decrease stroke volume, decrease BP.
80
Q

What results in increased contractility

A

Increased Stroke volume

81
Q

Epinephrine and Norepinephrine

A
  • Both alpha and beta agonists

- Will increase the force of contraction, heart rate, and constrict the veins and arteries.

82
Q

Baroreceptor Reflex

A
  • In the carotid sinus and the aortic arch there are specialized nerve terminals that can sense stretch in the vessel
  • If the arterial pressure increase the rate of firing in the baroreceptors increases
  • Also vice versa
  • Brain will recognize the decrease or increase in firing
  • Will either inhibit the parasympathetic and sympathetic system
83
Q

Afferent Arc of the Baroreflex

A

-Every reflex has an afferent arc. Information from receptor is sent up to the brain. Then the brain sends information via the autonomic system.

Afferent Arc - to the brain
Efferent Arc - to the blood vessel/organs/etc

84
Q

How Baroreceptor Reflex works

A

Decrease in arterial pressure –> decrease in Arterial Baroreceptors firing –> Decrease in parasympathetic outflow to heart –> increase in sympathetic outflow to heart, arterioles, veins –> thus increase in HR, Contractility, vasoconstriction, vasoconstriction –> Pressure goes up

85
Q

Effect of Baroreflex

A
  • Increase in HR, SV, and TPR
  • Increase venous pressure, during the diastolic phases the atrium will be more full, thus the ventricle will be more full
  • End diastolic pressure will increase. Stroke volume goes up, CO goes up.
86
Q

Autonomic Dysfunction

A

decreased working of the autonomic system

87
Q

When baroreceptors are cut

A
  • The systolic and diastolic fluctuate to high levels, resulting in high blood pressure
  • no change in mean BP. Baroreceptors do not control the mean BP
88
Q

Diuresis

A

kidney takes water out of the blood and puts it into the urine

89
Q

Renin-Angiotensin-Aldosterone (RAA) system

A
  • Arterial pressure falls, in the walls of the renal arteriole are special cells that make a hormone(actually enzyme) renin, that is dumped into circulation
  • Renin will travel in the blood until it finds Angiotensin (created by liver)
  • Turns it intro Angiotensin I, then travels to Lungs.
  • Ace in lungs turns it into Angiotensin II(will contrict arterioles, increase TPR, and MAP)
  • Angio II acts on particular parts of the brain so that it secretes a hormone called Anti-diuretic Hormone (ADH).
  • ADH will act on the kidney to decrease the amount of diuresis. Retain water in blood.

Third - Ang. II will bind to cells on the adrenal gland. WHich then secretes aldosterone which causes Na to stay in the blood stream. Causing more water stay in the blood –> BP goes up.

90
Q

Four major agents to bring down BP

A
  • Aldosterone receptor antagonist: will bind to aldo receptor in the kidney. Will occupy the receptor but not activate it. Will decrease water retention
  • Ace Inhibitor: Inhibits the enzyme that turns angiotensin into angio II. Body makes less Ang II –> lower BP

AT-II Receptor Blocker: Block all ang II receptors, stopping any of the above actions from happening

Renin Inhibitor: Inhibits the action of renin on angioten substrate to make Ang. I –> lower BP

Physiology 210 (5 decks)

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