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Boards: Cardiovascular > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

1
Q

Windkesssel Effect

A

Pulsatile outflow of LV converted to continuous flow by:
1. elastic properties of aortic wall, large arteries - store ejected blood so act as a reservoir
2. presence of resistance in peripheral vessels
3. prevention of retrograde flow by aortic valve

Stored blood forced out into peripheral vessels during diastole - responsible for ~50% of peripheral blood flow in most animals during normal HRs

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2
Q

Cross Sectional Area and Flow

A

o Significant resistance to flow in small arteries, increases in arterioles = SLOWS velocity of blood

Ensures blood flow through capillaries = continuous, slow: favors diffusional exchange of nutrients btw tissues, blood
* Velocity in capillaries (LJ) 0.03cm/s

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3
Q

Which has a larger SA - pulmonary capillary beds or systemic?

A

Pulmonary capillary beds (4000 cm2 SA)&raquo_space;> systemic capillary beds (2800 cm2 SA)

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4
Q

Vessel Types

A

o Elastic, Windkessel-type conduits = large arteries
o Resistance vessels = small arteries
o Sphincter vessels = arterioles
o Exchange vessels = capillaries
o Capacitance vessels = venules, veins
o Large conduits = veins
o Shunt vessels = arteriovenous anastomoses

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5
Q

Larger blood vessels (>100-200μm)

A

Macrocirculation

High pressure portion of circuit

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6
Q

Smaller Arteries

A

Greater % SmM vs elastic tissue –> increased control over vessel diameter, vascular resistance, regulation of blood flow

Densely innervation

Control distribution of blood flow

Site of 80% pressure drop btw aortic, VC

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7
Q

Resistance Vessels

A

Arterioles/metarterioles principal determinants of vol, distribution of blood flow: a1, a2 R
 Thick, muscular walls

> 50% SVR

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8
Q

Arteriovenous Anastomoses

A

bypass capillary, connect arterioles to venules, allow shunting of blood
 SmM
 Greatest numbers in skin, extremities: thermoregulation

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9
Q

Capillaries

A

Microcirculation: <100um

Includes terminal arterioles, capillary networks, venules

Single layer of endothelium, large surface area for exchange of O2/nutrients/CO2

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10
Q

Continuous, non-fenestrated capillaries

A

 Tight junctions
 Located in all tissues of body except epithelia, cartilage

Functional pore size of approximately 5nm; permits diffusion of water, small solutes, lipid soluble materials
* Glycocalyx prevents loss of larger molecules, blood cells

Breaks within interendothelial cell junctions as a result of trauma, inflammation = primary path for transvascular fluid filtration, increase porosity

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11
Q

Special continuous, non-fenestrated capillaries

A

Central nervous system, enteric nervous system, retina, thymus

Endothelial cells bound together by tight junctions with effective pore size of <1nm

Responsible for BBB

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12
Q

Fenestrated Capillaries

A

Present in skin CT, kidney intestinal mucosa, endocrine, exocrine gland, choroid plexus

Absorb interstitial fluid into plasma

Allow for absorption/rapid exchange of water and solutes

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13
Q

Discontinuous/Sinusoidal Capillaries

A

Discontinuous, characterized by gaps between adjacent endothelial cells

 interstitial fluid essentially part of plasma volume and sinusoidal tissues

Spleen, liver, bone marrow, endocrine organs
 allows plasma proteins secreted by liver cells to easily pass through sinusoids, into bloodstream through pores 20- 280nm

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14
Q

Veins, Venules

A

Low-resistance conduits for return of blood to RA

Normally contain 60-70% blood vol during resting conditions– capacitance altered by SNS activity
o Veins 30x more compliant than arteries

High population of a1, a2 R – mobilize blood when needed (splanchnic circulation)
o Venous resistance (VM tone) = principal determinant of venous return, CO

Heart cannot pump more blood than receives

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15
Q

Layers of the Heart

A

Endocardium
Myocardium
Epicardium
Visceral Pericardium
Pericardial Sac
Parietal Pericardium
Fibrous Pericardium
Mediastinal Parietal Pleura

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16
Q

Role of Fibrous Pericardium

A

limits sudden overdistention of heart chambers

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17
Q

Coronary Vascular Anatomy

A

LV free wall, IVS: paraconal br L coronary a
Subsinuosal coronary: extension of L circumflex, majority of LV
R coronary: RV free wall - dominant in cats, horses
L coronary: dominant except in cats, horses

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18
Q

S1

A

Closure of AV valves when ventricular pressure > atrial pressure

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19
Q

S2

A

passive closure of semilunar valves (aortic, pulmonic) when ventricular pressure decreases during diastole

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20
Q

R-L Shunting during Anesthesia

A

Bypasses lungs: deoxygenated blood returns to systemic circulation

PSNS increases during apnea –> bradycardia, increases PVR –> promotes development of R-L shunt

Slows inhalant induction - effect more pronounced with less soluble anesthetics

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21
Q

L-R Shunt

A

 Recirculates pulmonary venous (oxygenated) blood back into pulmonary circulation
 Tachycardia, decreased PVR, increase L-R shunting coincide with ventilation

Can increase speed of IV induction

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22
Q

Main Substrate used by heart

A

non-esterified fatty acids (60% O2 consumption)

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23
Q

Type A Hearts

A

Dogs, cats, primates, rats

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24
Q

Type B Hearts

A

Cows, birds, small ruminants, horses, dolphins

Extensive His Purkinje system throughout

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25
SmM Contraction
Involuntary non-striated muscle Controlled by:  Receptor activation  Mechanical stretch activation of actin and myosin  Change in membrane potential
26
Basic Mechanism of SmM
increase cytosolic Ca, CICR from SR/through Ca channels from extracellular space, phosphorylation of light chain of myosin (MLC), Ca-calmodulin activates myosin light chin kinase (MLC kinase), interaction of myosin/actin and contraction Contractile activity determined primarily by phosphorylation of light chain of myosin
27
Receptors Responsible for Ca Influx
1. Voltage operated Ca channels 2. Receptor Operated - blocked by Ca channel blockers 3. Storage operated Ca Channels
28
How Decrease Ca from Intracellular
PMCA (plasma membrane Ca-ATPase pump), SERCA (sarcoplasmic reticulum Ca-ATPase pump), Na/Ca exchanger, Cytosolic Ca binding protein
29
NE, epi, AngTII, endothelin
Promote VC by binding to Gq GPCR --> increase intracellular [Ca]
30
How Inhalants Depress Myocardial Activity
Decreases IC Ca concentrations via blocking Ca channels (especially VOCCs ) Activation of Katp channels - K exiting, hyperpolarizaition (also activated during hypoxia, ischemia, acidosis, shock)
31
SkM Features
--Striated actin/myosin arranged in sarcomeres: 2 tubules/sarcomere --Well developed SR, transverse tubules --Troponin thin filaments --Ca enters cytoplasm from SR --Cannot ctx without nerve stimulation
32
CaM Features
--Striated actin/myosin arranged in sarcomeres: 1 tubules/sarcomere --Moderately developed SR, transverse tubules --Troponin thin filaments --Ca enters cytoplasm from SR, ECF --CAN ctx without nerve stimulation
33
SmM Features
--Not striated: actin >>> myosin --Poorly developed SR, no transverse tubules --Contains calmodulin: when bound Ca, activates MLC-K --Ca enters cytoplasm from SR, ECF, mitochondria --Maintains tone in absence of nerve stimulation
34
Structure and Function of CaM
Striated, branched m cells, single nuclei  Branching allows for fast signal propagation, contraction in three directions
35
Intercalated Disks
Mechanical anchoring points for cytoskeletal proteins ensure transmission of contractile forces produced by individual cells Allow rapid cell to cell communication via easy diffusion of ions btw cells
36
Gap junctions (connexons)
intercalated disks ensure rapid electrical communication btw cells, allows myocardium to act as functional syncytium, low electrical resistance
37
Desmosomes
anchor points to bring cardiac m fibers together, would otherwise fall apart during ctx
38
Adherens junctions
mechanical intercellular junctions, link intercalated disk to actin cytoskeleton  Anchor point where myofibrils attached
39
CaM Contractile Units
CaM --> myofibrils --> myofilaments --> sarcomeres in series (actin, myosin)
40
CamM Thick Filament
Myosin
41
CaM Thin Filament
Actin 2a helical strands of g-actin, interacts with myosin molecules to form cross bridges, ~300 molecules Includes all the troponins
42
Tropomyosin
prevents free actin from interacting with myosin when CaM at rest, interspersed in actin filaments
43
Troponin
regulatory protein with 3 subunits 1. Troponin C 2. Troponin T 3. Troponin I
44
Troponin C
binds Ca2+ ions during activation, initiates configuration changes in regulatory proteins that expose actin site across from cross-bridge formation
45
Troponin T
anchors troponin complex to tropomyosin
46
Troponin I
participates in inhibition of actin-myosin interaction at rest
47
Titan
macromolecule that extends from Z disk to M line, contributes significantly to passive stiffness of CaM over normal working stage  Doesn’t allow to get flaccid btw beats
48
Three MOA to Decrease IC Ca in CaM
1. Increased activity of calmodulin - stimulates active extrusion of Ca by pumps in sarcolemma 2. Increased activity of phospholamban to increase Ca uptake by SR --Increased relaxation with beta stimulation 3. Enhanced activity of Na-Ca exchanger
49
Nerst Equation
Single ion’s equilibrium potential, equivalent to Vrev if channel singly selective for that ion
50
Goldman Katz Equation
 Combined equilibrium potential of all relevant (permanent) ions  Provides RMP  Also provides Vrev of multi-ion channels
51
RMP Cardiac Cells
RMP cardiac cells: -90mV vs -65mV for nerves/m Cells with more negative RMP have greater excitability, more rapid conduction velocity More negative: atrial cells, ventricular cells, Purkinje cells Less negative: SA, AV node cells; diseased myocardium
52
Speed of Cardiac APs
Cardiac APs (150-300ms) > nerve APs (1-3ms) DT prolonged plateau phase from changes in membrane permeability to calcium Also greater in magnitude change 130mV vs 80mV
53
Long QT syndrome
Related to repolarization currents (IK) DT importance in determining AP duration * Uncommon condition in people in which delayed repolarization of heart increased risk TdP predisposing to vfib Related to phase 3/outward movement of K
54
Absolute Refractory Period
200ms threshold for depolarization is infinite, ie no stimulus, no matter how great, will be able to make the myocyte depolarize again * VG Na channels: will not open until MP < -40mV
55
Relative Refractory period
50ms **stimuli of normal magnitude do not produce any depolarization, unnaturally large stimuli can produce depolarization of lower magnitude** * Fewer Na channels available so takes larger stimulus to activate, trigger depolarization * If depol does occur, still too few to make proper Phase 0 spike  lower amplitude phase 0
56
Functional/Effective Refractory Period
combo of absolute and relative; cell cannot produce AP that could depolarize surrounding muscle * Depol completely impossible or because ends up being so useless that cannot trigger depolar of adjacent cells
57
Supranormal Period
repolarization reaches nadir which slightly below RMP, creates hyperexcitable period during which weaker, subnormal stimulus could trigger depolarization and produce AP
58
RMP SA, AV Nodal Cells
max neg diastolic threshold -65mV
59
RMP Purkinje network, atrial specialized pathways
 Purkinje network, atrial specialized pathways -90mV
60
L Type Ca Channels
 AKA dihydropyridine R  Predominant Ca channels in heart, VG  Begin to open during AP upstroke (phase 0) when membrane depolarized to -10mV,  Blocked by Ca Channel Blockers **Long Lasting**
61
T Type Ca Channels
**Transient**  Open during phase 0 when membrane potential -60 to -50mV, VG  Not affected by catecholamines, Na channel blocks, Ca antagonists
62
T Type Ca Channels
63
Funny Current
Na, Ca, K - predominantly Na in PM cells Contributes to slow depolarization during diastolic interval Progressive decrease in membrane permeability to K, increased permeability to Na Also have changes in Ca permeability at end of diastole where increase in permeability/inward movement of Ca - contributes to diastolic depolarization Activated by hyper polarization
64
SaN
PM = determines HR) DT slow spontaneous diastolic depolarization of membrane, fastest in SA nodal cells  Cells usually reach TP, fire before any other cells
65
AVN
slowed as passes through AV node: small size of AV nodal cells, slow rate of rise of their AP, low RMP (-60mV) AV node delays transfer of cardiac excitation from atria to ventricles = allows atrial ctx to contribute to ventricular filling before ventricles begin to ctx
66
Why Pause at AVN (0.1msec)?
ATRIAL KICK, up to 20% of CO – DELAY IS IMPORTANT TO ALLOW ATRIA TO CONTRIBUTE TO VENTRICULAR FILLING AV nodal cells have faster depol than all other areas of heart except SA node  latent pacemaker
67
Ventricular Cells
last to depol, first to repol (short duration APs) AP ~1msec
68
Purkinje Cells
+midmyocardial cells at middle of ventricular walls have longest AP serve as physiological gates to prevent reentry, recycling of electrical impulses in ventricular myocardium
69
Overdrive Suppression
Purkinje cells have capacity to spontaneously depolarize via funny current, usually concealed by own slow depolarization rate (40-50bpm)
70
What are the two most proarrhythmogenic changes of the cardiac AP?
slowing of repolarization (triangulation), slowing of conduction
71
Triangulation
Altering duration, shape of AP, RP, impulse conduction velocity creates regional heterogenous differences Leads to creation of re-entry circuit
72
Altered Conduction
important parameter for determining product of conduction velocity x refractory period

Boards: Cardiovascular (11 decks)

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