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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
Q

SmM Contraction

A

Involuntary non-striated muscle

Controlled by:
 Receptor activation
 Mechanical stretch activation of actin and myosin
 Change in membrane potential

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26
Q

Basic Mechanism of SmM

A

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

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27
Q

Receptors Responsible for Ca Influx

A
  1. Voltage operated Ca channels
  2. Receptor Operated - blocked by Ca channel blockers
  3. Storage operated Ca Channels
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28
Q

How Decrease Ca from Intracellular

A

PMCA (plasma membrane Ca-ATPase pump), SERCA (sarcoplasmic reticulum Ca-ATPase pump), Na/Ca exchanger, Cytosolic Ca binding protein

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29
Q

NE, epi, AngTII, endothelin

A

Promote VC by binding to Gq GPCR –> increase intracellular [Ca]

30
Q

How Inhalants Depress Myocardial Activity

A

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
Q

SkM Features

A

–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
Q

CaM Features

A

–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
Q

SmM Features

A

–Not striated: actin&raquo_space;> 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
Q

Structure and Function of CaM

A

Striated, branched m cells, single nuclei
 Branching allows for fast signal propagation, contraction in three directions

35
Q

Intercalated Disks

A

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
Q

Gap junctions (connexons)

A

intercalated disks ensure rapid electrical communication btw cells, allows myocardium to act as functional syncytium, low electrical resistance

37
Q

Desmosomes

A

anchor points to bring cardiac m fibers together, would otherwise fall apart during ctx

38
Q

Adherens junctions

A

mechanical intercellular junctions, link intercalated disk to actin cytoskeleton
 Anchor point where myofibrils attached

39
Q

CaM Contractile Units

A

CaM –> myofibrils –> myofilaments –> sarcomeres in series (actin, myosin)

40
Q

CamM Thick Filament

A

Myosin

41
Q

CaM Thin Filament

A

Actin

2a helical strands of g-actin, interacts with myosin molecules to form cross bridges, ~300 molecules

Includes all the troponins

42
Q

Tropomyosin

A

prevents free actin from interacting with myosin when CaM at rest, interspersed in actin filaments

43
Q

Troponin

A

regulatory protein with 3 subunits

  1. Troponin C
  2. Troponin T
  3. Troponin I
44
Q

Troponin C

A

binds Ca2+ ions during activation, initiates configuration changes in regulatory proteins that expose actin site across from cross-bridge formation

45
Q

Troponin T

A

anchors troponin complex to tropomyosin

46
Q

Troponin I

A

participates in inhibition of actin-myosin interaction at rest

47
Q

Titan

A

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
Q

Three MOA to Decrease IC Ca in CaM

A
  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
Q

Nerst Equation

A

Single ion’s equilibrium potential, equivalent to Vrev if channel singly selective for that ion

50
Q

Goldman Katz Equation

A

 Combined equilibrium potential of all relevant (permanent) ions
 Provides RMP
 Also provides Vrev of multi-ion channels

51
Q

RMP Cardiac Cells

A

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
Q

Speed of Cardiac APs

A

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
Q

Long QT syndrome

A

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
Q

Absolute Refractory Period

A

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
Q

Relative Refractory period

A

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
Q

Functional/Effective Refractory Period

A

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
Q

Supranormal Period

A

repolarization reaches nadir which slightly below RMP, creates hyperexcitable period during which weaker, subnormal stimulus could trigger depolarization and produce AP

58
Q

RMP SA, AV Nodal Cells

A

max neg diastolic threshold -65mV

59
Q

RMP Purkinje network, atrial specialized pathways

A

 Purkinje network, atrial specialized pathways -90mV

60
Q

L Type Ca Channels

A

 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
Q

T Type Ca Channels

A

Transient

 Open during phase 0 when membrane potential -60 to -50mV, VG
 Not affected by catecholamines, Na channel blocks, Ca antagonists

62
Q

T Type Ca Channels

A
63
Q

Funny Current

A

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
Q

SaN

A

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
Q

AVN

A

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
Q

Why Pause at AVN (0.1msec)?

A

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
Q

Ventricular Cells

A

last to depol, first to repol (short duration APs)

AP ~1msec

68
Q

Purkinje Cells

A

+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
Q

Overdrive Suppression

A

Purkinje cells have capacity to spontaneously depolarize via funny current, usually concealed by own slow depolarization rate (40-50bpm)

70
Q

What are the two most proarrhythmogenic changes of the cardiac AP?

A

slowing of repolarization (triangulation), slowing of conduction

71
Q

Triangulation

A

Altering duration, shape of AP, RP, impulse conduction velocity creates regional heterogenous differences

Leads to creation of re-entry circuit

72
Q

Altered Conduction

A

important parameter for determining product of conduction velocity x refractory period

Boards: Cardiovascular (11 decks)

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