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Physiology > Combined Test 1 > Flashcards

Combined Test 1 Flashcards

1
Q

what determines coronary blood flow? what regulates it?

A
  • determines: aortic pressure- regulates: metabolic activity/changes in arteriolar resistance
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2
Q

when do you see a reversal in the blood flow of the left- but not right- coronary artery?

A

during max systolic pressure (isovolumetric contraction- rapid ejection) aka early systole

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3
Q

60-65% of coronary blood perfusion to LV muscle occurs during ______

A

diastole

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4
Q

Vessels in the endocardium or epicardium are more compressible? Which vessels are more dilated? Which is more at risk for ischemia?

A
  • endo to ALL
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5
Q

What compress endo/epicardium vessles?

A

Diastolic pressure and contraction

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6
Q

what is the relationship between blood flow and metabolic activity?

A

linear* increased metabolism, decreased resistance, increased blood flow

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7
Q

what are the metabolic substrates for the heart, and what is the largest consumer of O2?

A

fatty acids (LARGEST O2), carbs, ketones/lactate/proteins

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8
Q

how does the heart get more oxygen?

A

it is flow limited- must vasodilate

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9
Q

what is the equation for cardiac work, and which factor matters more?

A

cardiac work= MAP x systolic stroke volume (W=F*D)- pressure is more important

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10
Q

which factors affect myocardial oxygen supply?

A
  • diastolic perfusion pressure - coronary vascular resistance (external vs intrinsic (metabolites)) - O2 carrying capacity
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11
Q

which factors create largest O2 demand?

A
  • afterload- heart rate- contractility
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12
Q

what is ischemia, considering O2?

A

imbalance in the ratio of oxygen supply to oxygen demand; creates a relative lack in blood flow- excessive O2 demand is NEVER the primary cause (always too little supply)

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13
Q

what is coronary steal?

A

an increase in blood flow to one region can cause a decrease in flow to another- * problematic with vasodilation if there is a stenosis *

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14
Q

when would coronary steal present clinically?

A
  • exercise-induced ischemia- stress testing- peripheral arterial disease
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15
Q

What happens to skeletal muscle circulation during exercise?

A
  • the flow oscillates- overall, there is a significant reduction in resistance to blood flow to vasodilation
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16
Q

Skeletal flow can increase ___ time during exercise, which is called _____. It constitutes the ____ vascular bed in the body. Which type of muscle has more vascular supply- tonic or phasic?

A

20 active hyperemialargesttonic

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17
Q

What is the main vasodilator- working against sympathetics- in skeletal muscle?

A

adenosine

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18
Q

Skeletal muscle vasculature is primarily innervated by _____ fibers

A

sympathetic adrenergic

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19
Q

Ach causes ___ by acting on ___ coupled to ___

A

vasodilation muscarinic (on endothelials) NO production

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20
Q

Epinephrine from ____ causes ____ at low concentrations through activating _____, but _____ at high concentrations through activating ____

A
  • adrenal medulla- vasodilation - beta-2 adrenergic receptors- vasoconstriction - alpha adrenergic receptors
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21
Q

The brain primarily uses _____ metabolism of _____. How metabolically active is it?

A

aerobic metabolism of glucosemost metabolically active tissue in the body

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22
Q

What is the BBB due to? What can cross?

A
  • endothelial tight junctions- basement membrane- neuroglial processes - metabolic enzymes - lipid soluble substances- O2, CO2, ethanol, steroids, glucose
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23
Q

What is CPP? If CPP falls, what happens? What reduces CPP?

A
  • cerebral perfusion pressure- CPP= MAP- intracranial venous pressure - vasodilation - reduced by decrease in MAP or increase in intracranial pressure
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24
Q

what is the monroe-kellie doctrine?

A

brain volume + cerebral vascular volume + CSF volume= constant

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25
Q

What happens as CSF pressure rises?

A
  • increase CSF pressure- cerebral blood flow decreases (veins compressed) - metabolic autoregulation dilates the arteries- this only works up until a certain pressure, where the arteries become compressed
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26
Q

Cerebral blood flow is very sensitive to which metabolite?

A

PCO2

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27
Q

An increase in pH (hyperventilation) causes what? This helps with what clinical scenario?

A
  • vasoconstriction & decreased blood flow- cerebral edema (high intracranial pressures)
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28
Q

mechanism for nitric oxide

A
  • causes vasodilation of smooth muscle - increases cGMP and PKG- increases phosphorylation of MLCK- decreases phosphorylation of myosin light chain
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29
Q

what is the cushing response?

A

with elevated intracranial pressure, you see - high blood pressure (medulla sympathetics)- low heart rate (parasympathetics)

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30
Q

when does the cushing response occur?

A

when CSP (cerebral spinal pressure) is greater than the mean arterial pressure

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31
Q

Pulmonary circulation is a ____ pressure, ____ volume system, ___ resistance; mean pressure gradient= ____

A

low pressure, high volume, low resistancemean pressure gradient 6 mm Hg

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32
Q

Pulmonary arteries are ___ compliant than regular arteries because____

A

7x more; they lack smooth muscle

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33
Q

Pulmonary capillaries represent ___ of the vascular resistance

A

40%

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34
Q

T/F Pulmonary vessels autoregulate

A

F

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35
Q

During inspiration, negative pressure ______’s extra-alveolar vessels and _____ resistance in alveolar vessels - net effect on resistance = ?

A

distends; increases net effect- no change!

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36
Q

intravascular (hydrostatic) pressure is greatest at which part of the lung? what does this cause?

A

bottom waterfall effect

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37
Q

what happens in zone 1?

A

alveolar pressure exceeds arterial and veous pressures, causing capillaries to collapse- exists w/ hypotension or positive pressure mechanical ventilation

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38
Q

what happens in zone 2?

A

alveolar pressure exceeds venous pressure but does not exceed arterial pressure; capillaries are partially collapsed, is the upper 1/3rd of lung

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39
Q

what happens in zone 3?

A

arterial and venous pressures exceed alveolar pressure; flow depends on AV pressure gradient

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40
Q

primary function of cutaneous circulation

A

maintain a constant body temperature - provides transport of heat to the body surface for exchange with the environment

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41
Q

what is apical skin?

A
  • high surface-volume ratio that favors heat loss- has lots of AV anastomoses called glomus bodies
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42
Q

what is nonapical skin?

A
  • lacks AV anastomoses- innervated by sympathetic fibers- postganglionics release Ach; vasodilation
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43
Q

neural control of apical skin

A

sympathetic adrenergic nerves that produce vasoconstriction of cutaneous vessels (withdrawal produce passive vasodilation)

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44
Q

neural control of nonapical skin

A
  • sympathetic vasoconstriction (NE) - active vasodilation via cholinergic fibers via bradykinin
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45
Q

temperature regulation (what kind?) is primarily controlled by major sensory sites in the ______ and less by receptors in the spinal cord

A

core body temperature; hypothalamus

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46
Q

fetal circulation pathway

A

fetal branch villi- umbilical vein- ductus venosus- IVC- RA- foramen ovale- LA-LV- aortasome blood goes RA- RV-pulm artery- ductus arteriosis- systemic circulation

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47
Q

valves close, pressure changes, pipes shut

A

valves close- foramen ovale
pressure changes- atria
pipes shut- ductus venosus & ductus arteriosus

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48
Q

difference between HbF and HbA and why?

A

HbF has greater affinity for O2 due to DpG shifting O2 dissociation curve left- more saturation at lower pressures

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49
Q

umbilical arteryumbilical veinductus venosusductus arteriosus

A

umbilical artery- medial umbilical ligament
umbilical vein- ligamentum teres
ductus venosus- legamentum venosus
ductus arteriosus- ligamentum arteriosum

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50
Q

what happens with skin circulation and exercise?

A

sympathetics want to vasoconstrictinternal metabolic heat stimulates cutaneous vasodilation

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51
Q

what does the arrangement of vessels within the intestinal villus form?

A

contercurrent flow system; arteries and venules run parallel to each other- solutes such as sodium dissolve from the arteries back to the venules to increase osmolarity/blood flow

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52
Q

What ist he portal system?

A

1- portal vein- blood from intestine/stomach/pancreas (only a few mmHg higher than IVC)2- liver capillaries- blood from portal vein3- hepatic vein- liver capillaries 4- IVC

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53
Q

metabolic control of splanchnic circulation

A

increase metabolismO2 decreasesmetabolites (CO2, H+, adenosine) increasevasodilation (moderate autoregulation)

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54
Q

hormonal control of splanchnic circulation

A

cholecystokinin & neurotensin increase vasodilation

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55
Q

neural control of splanchnic circulation

A
  • sympathetic vasoconstriction via NE acting on alpha adrenergic receptors on vascular smooth muscle (also have beta receptors) - parasympathetics act indirectly by contacting sympathetics in intestinal wall & stimulates motility
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56
Q

what is postprandial hyperemia?

A

after eating, get increase in intestinal blood flow due to metabolic/hormonal/neural/mechanical influences

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57
Q

what is the equation for ejection fraction?

A

EF= EDV-ESV/EDV * 100 (normally 60%)

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58
Q

what is the ejection fraction a clinical index of?

A

left ventricular contractility

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59
Q

systolic heart failure

A

decreased contractility (depends on activity)- shifts contractility line down

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60
Q

diastolic heart failure

A

decreased compliance, reduced preload (can’t fill normally because volume creates more pressure) - shift diastolic pressure-volume curve up

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61
Q

factors that determine preload

A
  • pressure gradient from atria-ventricle - time for ventricular filling (hr)- ventricular compliance - atrial function (kick)
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62
Q

factors that determine contractility

A
  • sympathetic nerve activity- drugs (digitalis) - disease (infarct)
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63
Q

factors that determine afterload

A
  • aortic pressure (hypertension) - ventricular outflow tract resistance (valvular or subaortic stenosis) - ventricular size- dilated hearts= larger afterload
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64
Q

venous return

A

rate at which blood returns to the thorax (central venous pool) from the periphery

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65
Q

central venous pool

A

the volume of blood enclosed by the right atrium and great veins (IVC, SVC)

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66
Q

cardiac output and what it equals

A

rate at which blood leaves CVP and is pumped out of the heart; equals venous return

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67
Q

relationship between cardiac output and central venous pressure? which variable is independent? what is this called?

A

as you lower cardiac output (& venous return), the blood backs up in the central venous pool & you get a higher central venous pressure up CO/VR, down CVP (inverse relationship)CO is the independent variable vascular function curve

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68
Q

what is Pmc? what is it a relationship between? what is it normally?

A
  • mean systemic circulatory pressure- the pressure in the venous system that occurs when the heart stops; - relationship between volume of blood and the capacity of the system (venous tone)- 7 mmHg
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69
Q

what happens when CVP= Pmc?

A

blood flow ceases- have no gradient for return

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70
Q

if you increase cardiac output, what happens?

A

decrease CVP, increase venous return (via pressure gradient)

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71
Q

what happens at negative CVP?

A

large veins collapse

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72
Q

which curve does transfusion shift?

A

vascular function curve - higher CO for lower pressure

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73
Q

which curve does sympathetic stimulation shift?

A

cardiac function curve- increases venous tone which increases venous return - higher CO for lower pressure (shifts up and left)

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74
Q

increase venous return by increasing peripheral venous pressure (PVP)

A
  • increased sympathetic venoconstriction - increased skeletal leg pump - increased blood volume - cardiac contraction
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75
Q

increase venous return by decreasing central venous pressure (CVP)

A
  • respiratory pump activity (decreased intrathoracic pressure)- cardiac suction (heart going from circular to oblong)
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76
Q

how do valves change venous return?

A

maintain pressure gradient between peripheral and central venous pools

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77
Q

where do you measure CVP (central venous pressure) graphically?

A

intersection of vascular function curve and cardiac function curve

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78
Q

which curve does heart failure shift?

A
  • cardiac function curve- shifts down progressively - hypervolemia also shifts vascular function curve out
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79
Q

2 main things that shift venous function curve

A

blood volumevenous tone

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80
Q

what happens with hemmorage?

A
  • shifts the venous function curve down;- sympathetics boost it back up AND boost the cardiac function curve to give you same CO at reduced CVP
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81
Q

what is Poiseuille’s law?

A

flow= (change in pressure)/(resistance)ORflow=(change in pressure * pi * r^4)/ (8Lviscosity)

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82
Q

what is the main way in which flow is regulated?

A

by changing vessel radius (r^4)

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83
Q

what is viscosity; what is the equation; how does it relate to velocity, hematocrit, and radius

A
  • lack of slipperiness- viscosity= sheer stress/sheer force (p/v)- inverse relationship w/ velocity- direct relationship with hematocrit - direct relationship with radius due to axial streaming
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84
Q

what is the definition of a non-newtonian fluid?

A

a fluid whose viscosity changes based on sheer stress (pressure) and force (velocity)

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85
Q

as a vessel diameter gets smaller, hematocrit _________ because of ________

A

decreases; plasma skimming

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86
Q

laminar vs turbulent blood flow

A

laminar- parallel concentric layersturbulent- disorderly patterns (murmurs, endothelial damage, thrombi); leads to Krotokoff sounds

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87
Q

what is the reynold’s # and its equation?

A
  • propensity for turbulent blood flow- R#= (densitydiametervelocity)/(viscosity)
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88
Q

what is Bernouilli’s principle and its equation?

A

in CONSTANT FLOW system (aka there are no escape routes), total energy remains constant total energy = potential energy + (1/2)*(density *velocity^2)aka if blood is going faster, will have decreased lateral pressure on the walls

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89
Q

what is the laplace relationship and its equation?

A
  • the force ripping the balloon apart - wall tension= (pressure * radius)/wall thickness
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90
Q

what happens with an aneurysm?

A

decreased velocityincreased pressureincreased radiusdecreased wall thicknessALL increase wall tension

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91
Q

example of low wall tension

A

capillaries in feet- have small radius, can resist a lot of force

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92
Q

what allows arterioles and precapillary sphincters to control vessel diameter and blood flow?

A
  • a high wall thickness/radius ratio; this provides low wall tension (laplace)- also have low volume-high pressure- low compliance- high resistance
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93
Q

cross sectional area and the velocity of blood flow

A

total cross sectional area is inversely related to the velocity of blood flow

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94
Q

what holds 60% of blood volume

A

veins (larger cross sectional area than arteries)

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95
Q

series vs parallel resistance

A

-series- add them up (think vessles- aorta to large arteries to capillaries to arterioles, etc.)- parallel- less than an individual- (think organs- open more up, have less resistance)); inverse- 1/r1 + 1/r2 etc

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96
Q

what is pulse pressure and where does pulse pressure become greater?

A
  • systolic-diastolic pressure- further you go away from the heart- greatest in ankle- large in arteries
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97
Q

what is mean arterial pressure? what is MAP determined by? what happens to it throughout the circulatory system?

A
  • avg pressure in the aorta and proximal arterial system during one cardiac cycle - diastolic pressure + 1/3 PP- declines- driving force- greatest in aorta?
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98
Q

3 layers (‘tunica’) of arterial wall

A
  • intima: connective tissue, endothelials, IEL- media: smooth muscle & EEL- adventitia- connective tissue w/ vasa vasorum, innervation
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99
Q

relationship between compliance and pressure

A

higher compliance (e.g. elastin), lower pressure

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100
Q

wall thickness/diameter ratio tells you what

A

greater ratio, better control of the system- greatest in arterioles, provides lots of resistance

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101
Q

where are continuous capillaries found?

A

muscle, connective tisues

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102
Q

where are fenestrated capillaries found?

A

kidney, intestines

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103
Q

where are discontinuous/sinusoidal capillaries found?

A

liver, bone marrow, spleen

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104
Q

what is the ‘windkessel’/hydraulic filtering?

A

when the aortic valve closes, the recoil of the aorta wall recoiling (was pushed out by systolic pressure) sends a second wave of pressure throughout the system, maintaining diastolic pressure

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105
Q

relationship between compliance and pulse pressure

A

low compliance- high pulse pressure- high afterload- high O2 consumption

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106
Q

what is pressure pulse?

A

the wave of energy that passes through the aorta at 5 m/sec and increases to 10-15 m/sec in arteries- velocity increases as compliance decreases

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107
Q

what are some specific determinants of mean arterial pressure?

A
  • cardiac output (hr * sv)- peripheral resistance(& baroreceptor, exercise, disease)- blood volume- arterial compliance
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108
Q

primary determinants of systolic & diastolic pressure?

A

systolic- cardiac outputdiastolic- peripheral resistance

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109
Q

if you decrease compliance, what happens to pulse pressure?

A

decrease compliance, increase pulse pressure

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110
Q

increase resistance, what happens to pulse pressure?

A

increase diastolic pressure (and some systolic)

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111
Q

what regulates peripheral arterial resistance?

A

changes in the arteriolar radius (viscosity would, but doesn’t change)

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112
Q

two types of ways to change arteriolar radius?

A

local- myogenic, endotheial, metabolites global (extrinsic)- baroreceptor, hormonal, sympathetics (aka not specific)

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113
Q

which is the main player of the autonomic nervous system in regulating mean arterial pressure?

A

sympathetics- acts on heart, veins, arterioles (increases HR, contractility, veno/vasoconstiction)- increasing CO increases BP

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114
Q

changes that occur during exercise

A
  • cardiac output rises (increase in contractility and hence stroke volume) BUT when HR reaches max, SV decreases - systolic pressure rises (increase in SV) - peripheral resistance decreases (skeletal capillaries open up) - enhanced O2 extraction- increases venous return (muscle and respiratory pump, venoconstriction)- pulse pressure widens - MAP increases- more time in systole
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115
Q

structures of microcirculation

A

precapillary resistors (arterioles, metarterioles, sphincters), exchange vessels, and venules

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116
Q

characteristics of capillary blood flow

A
  • slow- intermittent, not uniform/1 direction- follows pressure gradients
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117
Q

what is a Rouleaux formation?

A
  • stacks of RBCs- blood cells squeezing through capillaries at an angle, touching allows for good gas exchange
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118
Q

pressure gradients in capillaries

A

hydrostatic- 32 to 15osmotic- 25

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119
Q

what is the main force that holds things in? what is the most clinically relevant protein and what does it attract?

A
  • plasma osmotic (oncotic) pressure- albumin- attracts sodium (and water back into blood); produced by liver
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120
Q

what determines capillary hydrostatic pressure?

A

pre and post capillary resistance to arterial and venous flow

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121
Q

what happens when you decrease the pre/post capillary resistance ratio?

A
  • decrease pre resistance- more water flowing in OR- increase post resistance- less water able to flow out- OVERALL increase capillary hydrostatic pressure
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122
Q

when hydrostatic pressure is greater than osmotic pressure, you get

A

filtration

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123
Q

examples of vasodilators

A

prostacyclins, EDRF, NO, adenosine, H+, CO2, K+

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124
Q

examples of vasoconstrictors

A

endothelin (ET)

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125
Q

important structural features of lymphatic system

A
  • unidirectional flow of plasma & protein- valved, thin walls- non-fenestrated, no smooth muscles- return to subclavian veins
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126
Q

factors governing lymph flow

A
  • amount of filtration- skeletal muscle activity- valves
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127
Q

specific causes of edema

A
  • reduction in plasma protein (albumin- liver failure), renal disease- increase cap. hydrostatic pressure (congestive heart failure)- increased permeability of membrane (burns)- lymphatic obstruction (surgery)
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128
Q

what is edema?

A

excess fluid accumulation in interstitial space

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129
Q

which has a greater influence on hydrostatic pressure- arterial or venous pressure?

A
  • venous; excessive arterial pressure is normally dissipated by resistance
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130
Q

what is resting sympathetic tone and what is it due to

A
  • vascular constriction under resting conditions (basal tone) plus a small level sympathetic nerve activity due to being awake- due to tonically released norepinephrine
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131
Q

active vs passive mechanisms

A
  • can be sympathetic or parasympathetic - active- change in resistance away from basal arterial tone- passive- change in resistance towards basal tone
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132
Q

two types of inputs

A

sympathetic adrenergic- increases resistancesympathetic cholinergic- decreases resistance

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133
Q

which type of sympathetic fibers cause active vasodilation?

A

sympathetic cholinergics (release Ach as opposed to Ne)

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134
Q

what are alpha-1 receptors?

A
  • adrenergic receptors - on vascular smooth muscles- cause vasoconstriction - not on coronary/cerebral vessels (never want to constrict flow to the brain or the heart)
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135
Q

what are beta-2 receptors?

A
  • adrenergic receptors- on heart, are secondary receptors that stimulate heart rate and contractility- on smooth muscles, cause vasodilation
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136
Q

baroreceptors- anatomy

A

located on carotid sinus (MOST BLOOD FLOW IN BODY) & aortic arch (structures with LESS vascular smooth muscle)

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137
Q

baroreceptors- mechanism

A
  • are mechanoreceptors (respond to stretch)- fire more frequently by an increase in arterial pressure (vice-verse for decrease) - join 9&10 to medulla - decrease in stretch/firing= increases sympathetics and inhibits parasympathetics
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138
Q

ways sympathetics/PS change via baroreceptor

A

1) peripheral vasoconstriction (sympathetics)2) increase in heart rate (s and ps)3) increase in contractility (s)

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139
Q

baroreceptors respond to changes/absolute pressure and are more responsive to phasic/constant pressure

A

changes & phasic

140
Q

what are chemoreceptors activated by?

A

low arterial PO2**, high arterial PCO2 (shifts curve up), and high H+

141
Q

at a low CO2 concentration, receptors are ___ sensitive to a drop in O2

A

less

142
Q

what do chemoreceptors stimulate?

A

vasoconstriction (sympathetics) bradycardia (parasympathetics) BUT this is overruled by respiratory system which promotes tachycardia (stretch receptors in the lungs inhibit vagal nerve activity)

143
Q

what is the hormonal control of the circulator system? over what time frame and circumstances does it take place?

A
  • renin-angiotensin-aldosterone- dehydration or heart failure over weeks
144
Q

RAA pathway

A
  • increase in fluid volume- low arterial pressure (baroreceptors)- renin is released from JGA kidney cells in afferent arterioles - renin converts angiotensinogen to angitensin 1- ACE enzymes in lungs & kidneys convert 1 to 2- result in vasoconstriction of renal vessels- stimulates aldosterone release which pulls Na back into blood from kidneys- acts on hypothalamus to stimulate thirst and ADH
145
Q

local mechanisms responsible for vascular resistance

A

autoregulation (myogeneic, metabolic)endothelialmechanical

146
Q

what is autoregulation? what are the two primary mechanisms?

A
  • when an abrupt increase in flow caused by an increase in arterial pressure is counteracted by an increase in resistance to maintain constant flow - myogenic (smooth muscle contracts in response to stretch)- metabolic (production of adenosine, H+, Co2= VASODILATORS)
147
Q

auto-regulation among different organs

A

strong- heart, brain, kidney, skeletal muscleweak- splanchniclittle- skin, lungs

148
Q

what is it called when you see a decreases in diameter in response to an increase in pressure with or without the endothelium

A

autoregulation

149
Q

what is it called when you see an increase in diameter in response to an increase in pressure gradient, but only with endothelium; what it is due to

A

endothelial-mediated mechanism (exercise); due to increase in sheer stress of blood, result of increase in EDRF

150
Q

what is active hyperemia?

A

increased blood flow caused by increased tissue activity (skeletal and cardiac muscle)

151
Q

what is reactive hyperemia?

A

overshoot of blood flow in response to a metabolic debt created by a temporary occlusion

152
Q

how does mechanical activity regulate blood flow?

A

increase in tissue pressure (think during a bicep curl) compresses small vessels and alters blood flow

153
Q

where does mechanical activity regulate blood flow

A

muscle contraction, alveolar pressure, tumors, aortic stenosis

154
Q

what is shock a primary reaction to?

A

cardiovascular system is unable to supply enough blood to the body; LOW BLOOD PRESSURE

155
Q

Refractory characteristics of slow vs fast APs

A

slow- time dependent- Ca2+ - longerfast- voltage dependent- Na+

156
Q

R on T phenomenon- PVCs

A

a premature beat (R wave) occurs during the relative refractory period of the previous beat (T wave) aka premature ventricular contraction- PVCs= polymorphic ventricular tachycardia

157
Q

what is special about the refractory period of the AV node

A

have post-repolarization refractoriness- protects the ventricles during atrial fibrilation - depends on Ca2+ channels

158
Q

In atrial fibrillation, what is determining the rate and rhythm of the ventricular activation?

A

AV node refractory characteristics

159
Q

How do you slow ventricular rate in patient with atrial fibrilation?

A

Calcium channel blocker or Beta blocker

160
Q

as HR goes up, which part of the cardiac cycle shortens most

A

diastole

161
Q

action potential duration equals what part of the cardiac cycle and what part of the EKG

A

systole Q-T

162
Q

what causes prolonged Q-T syndrome (T wave is super late)

A

acquired- bradycardia, hypokalemia, quindinecongenital- defects in sodium and potassium channels e.g. Torsades (doesn’t repolarize normally is AP is too long, can be initiated by R on T)

163
Q

hierarchy of cardiac pacemaker activity

A

arranged based on inherent beating rate: SA node > latent atrial pacemakers > AV nodal/His bundle (junctional) > bundle branches > Purkinje’s

164
Q

diastolic depolarization- SA node

A

-T-type Ca current (at - voltages, Ca in) - hyperpolarization-activated inward current od sodium (funny channels) - deactivation of K+ current- inward Na/Ca exchanger

165
Q

diastolic depolarization- Purkinje fibers

A
  • hyperpolarization-activated inward current of sodium (funny channels) - deactivation of K+ current
166
Q

things that change heart rate

A

1- slope of diastolic depolarization 2- change in maximum diastolic potential (resting potential)3- change in threshold 4- change of pacemaker

167
Q

how would vagal nerve stimulation affect an EKG recording?

A

would have a longer R-R (less bpm)

168
Q

what is sinus arrhythmia

A

variability in pacemaker cycle length caused by respiratory changesinspiration- increase HR- inhibits PS nerve activityexpiration- decreases HR- stimulate PS nerve activity

169
Q

heart rate is slower during expiration/inspiration

A

expiration

170
Q

molecular reasons for cardiac arrhythmia

A

impulse formation, conduction, or both

171
Q

electrical mechanisms responsible for dysrhythmias

A

altered automaticity, re-entry of excitation, triggered activity

172
Q

causes of tachy-dysrhythmias

A

NE (sympathetics)stimulants (caffeine)stretching (aneurism) sick sinus syndrome, fever, hyperthyroidism (BUSH)

173
Q

causes of brady-dysrhythmias

A

drugs (beta blockers, calcium channel blockers, digitalis) barbiturates, anestheticsishchmia/infarctsick sinus syndromeaging

174
Q

causes of re-entry excitations

A

ischemiainfarctioncongenital bypass tracts (WPW)

175
Q

causes of DADs

A

“Delayed afterdepolarization” digitaliselevated catecholaminesrapid heart beatEVERYTHING TOGETHER

176
Q

causes of EADs

A

“Early after depolarization” acidosis (ischemia) hypokalemiaquinidineslow heart rates

177
Q

3 requirements for re-entry of excitation

A

1- geometry for conduction loop2- slow or delayed conduction3- unidirectional conduction block

178
Q

anti-arrhythmic therapies

A

1- drugs (Ca channel blockers, beta blockers)2- radio frequency ablation3- DC cardioversion4- implantable cardioverter-defibrillator

179
Q

PR interval length

A

0.12-0.2 seconds

180
Q

QRS complex length

A

0.07-0.1 seconds

181
Q

QT interval length

A

0.25-0.43 seconds

182
Q

cardiac E-C coupling steps (CICR)

A

1) AP goes down into T-tubules2) Depolarization activates L-type Ca2+ currents on sarcolemma & t-tubule membrane3) Influx of Ca2+ binds to SR and opens Ryr channels 4) Released Ca2+ binds to troponin C5) Relaxation occurs when Ca2+ is removed

183
Q

structure-function EC coupling: sarcolemma

A
  • propagates action potentials- controls Ca2+ influx via slow inward Ca2+ current
184
Q

structure-function EC coupling: T-tubules

A
  • transmits electrical activity to cell interior - located at Z-lines
185
Q

structure-function EC coupling: SR, terminal cisternae

A
  • where Ca2+ influx triggers opening of Ca2+ release channels
186
Q

structure-function EC coupling: SR, longitudinal cisternae

A
  • cite of Ca2+ re-uptake to initiate relaxation
187
Q

structure-function EC coupling: troponin C

A
  • Ca2+ receptor on actin (contractile protein)
188
Q

cardiac vs skeletal muscle: size, connection, activation

A

size: cardiac are much smallerconnection: cardiac are electrically coupled (syncytium) vs individual muscle cells activation: cell to cell conduction vs Ach transmission at NMJs

189
Q

cardiac vs skeletal muscle: contraction, contraction amplitude, summation, metabolism

A

contraction: CICR vs voltage-sensors on Ca2+ channelsamplitude: Ca2+ influx and SR content vs frequency of APssummation: no summation vs tetanus metabolism: aerobic (35%mit) vs anaerobic (2% mit)

190
Q

what is contractility, and can you change the strength of a contraction without changing it?

A

contractility- the inherent ability of actin and myosin to form cross-bridges and generate contractile force; determined by intracellular Ca2+ YES

191
Q

what are catecholamines

A

NE (neurotransmitter) and E (hormone)

192
Q

mechanism of catecholamines

A

1) bind to Beta1 receptors on sarcolemma 2) activation adenyl cyclase to increase cAMP 3) cAMP activates PKA4) PKA phosphorylates lots of stuff

193
Q

what does PKA phosphorylate in the catecholamine cascade?

A

1- Ca2+ channels- increases calcium influx2- phospholamban- increases SRCA rate (relaxation) 3- troponin I- reduces troponin C’s affinity for calcium 1&2 increase strength of contraction2&3 decrease time course of relaxation

194
Q

mechanism of calcium channel blockers

A

1- plugs up Ca+ influx2- decreases SR release of Ca2+- leads to less contraction (VASODILATION) 3- inhibition of slow inward Ca2+ channel inhibits conduction of AV node, blocks SVT

195
Q

3 factors that change muscle contraction via a change in contractility

A

1) catecholamines- sympathetics2) cardiac glycosides (dig)3) Ca2+ channel blockers (vasodilator, blocks SVT)

196
Q

Cycle length influences contraction amplitude by altering _______ by altering the time available for intracellular Ca2+ handling

A

contractility

197
Q

positive staircase- as heart rate increases, the strength of the contraction ____

A

increases- greater Ca2+ influx at higher HR, less time for Ca2+ efflux; increased SR content and release

198
Q

premature beat results in a ___ than normal contraction

A

smaller- less time for recovery of slow inward Ca2+ current & SR release channels & re-organization of terminal cisternae - gives you a smaller CICR release

199
Q

what is a PESP

A

post-extrasystolic potentiation- stronger than normal contraction of the heart following a premature beat- more time for recovery of Ca2+

200
Q

signs of A-fib w/ radial pulse

A

fast heart rate (tachycardia), irregular speed of heart rate, force for each beat is different ** because of force-frequency relationship, different amounts of Ca2+ causing different forces of contraction** skipped beat is b/c not enough pressure to open aortic valve ** thumping is a PESP

201
Q

contractility of the heart is ____ with a premature beat

A

reduced

202
Q

turn on an electric stimulator (in a lab) to increase heart rate, what does it look like?

A

premature beat (but think stair-case effect- slowly recovers)

203
Q

four factors that determine cardiac output

A

1) heart rate2) myocardial contractility3) preload4) afterload

204
Q

what is preload dependent on? if preload were low, what would the treatment be?

A
  • end-diastolic volume (the amount of ventricular filling) - generates passive tension - give more volume
205
Q

afterload is any force that _____

A

resists muscle shortening e.g. arterial pressure(the load on the muscle after contraction is initiated)

206
Q

a premature beat is a _____ contraction

A

isometric

207
Q

if compliance is low, the tissue is _____; aka _____

A

stiff; heart

208
Q

the slope of the resting tension curve is primarily determined by

A

muscle compliance

209
Q

the slope of the active tension curve is primarily determined by

A

muscle contractility

210
Q

what is resting diastolic tension

A

the amount of tension that develops passively by stretching the muscle (increasing preload)initial myocardial fiber length= EDV

211
Q

what is active systolic tension

A

the amount of isometric tension that is developed by muscle contraction at a particular preload

212
Q

stretching cardiac muscle …

A

a) creates more optimal overlap between the thick and thin filaments b) increases Ca2+ sensitivity of myofilaments

213
Q

_____ increases the max slope of the systolic tension curve, and _____ decreases it

A

sympathetics; heart failure

214
Q

an increase in preload ____ the amount of muscle shortening

A

increases

215
Q

an increase in afterload ___ the amount of muscle shortening

A

decreases

216
Q

A positive increase in contractility changes what? (tension, relaxation, muscle shortening, velocity of shortening)

A
  • raises peak isometric tension - enhances the rate of relaxation (sympathetics) - increases the amount of muscle shortening- increases the velocity of shortening
217
Q

afterload is synonymous with what

A

force

218
Q

increasing afterload

A

decreases the velocity of muscle shortening decreases the amount of muscle shortening

219
Q

at a given afterload, an increase in preload

A

shifts the curve right; increases the velocity of shortening and the max isometric force

220
Q

at a given afterload, an increase in contractility

A

shifts the curve up and to the right; increases the velocity of shortening and the max isometric force

221
Q

EKG inferior view of the heart

A

leads 2, 3 and aVF

222
Q

EKG lateral view of the heart

A

leads 1, aVL, V5, V6

223
Q

EKG anterior view of the heart

A

leads V3, V4

224
Q

EKG septal view of the heart

A

leads V1, V2

225
Q

which electrode is most parallel to mean frontal plane vector? and which direction is it in?

A

II, down and left

226
Q

order of ventricular depolarization

A

interventricular septum (down-right), apical depolarization (down-left), endocardial surface (down-left)

227
Q

why is the vector of repolarization the same as depoarlization?

A
  • repo starts where depo ends- repo goes from positive to negative, so vector is switched
228
Q

what is the last part of the heart to depolarize?

A

epicardial surface of the left ventricle

229
Q

where is the AP slower- endo or epi- and why?

A

endocardial surface- it has less Ito K+ channels, repolarization takes longer

230
Q

normal angles for Einthoven’s triangle

A

-30* - 105*

231
Q

if the mean frontal plane vector is more negative than -30, which kind of deviation is it?

A

left axis

232
Q

how to use hexaxial reference to approximate the MFPV

A

1- pick smallest recording of the 122- take line perpendicular to that3- see if that line is + or - (pointing right or left) 4- use that line to approximate vector

233
Q

einthoven triangle method

A

1- sum blocks up and down for q+rs+t for two leads (1+3=2)2- plot value on triangle

234
Q

things that skew MFPV

A

left ventricular hypertrophypulmonary hypertensionbundle branch block (right deviation w/ right block)

235
Q

which part of conduction does hypokalemia affect most and what happens?

A

Purkinje fibers- AP lengthens and u wave pops outU wave- after T, repolarization of purkinjes

236
Q

if all the QRS complexes are taller, what do you suspect?

A

hypertrophy- more cells= more current

237
Q

phases of the cardiac cycle

A

atrial systole (last squeeze)isovolumic contraction (**all valves closed)ejection- rapid and reducedisovolumic relaxationfilling- rapid & reduced

238
Q

units for pressure, aortic blood flow, ventricular volume, time

A

mm Hg (0-120)L/min (0-5)ml (20-38)0-0.8 seconds

239
Q

ACV waves

A

A- atrial contractionc- ventricular contractionv- filling & emptying of atrial chamber

240
Q

3rd heart sound

A

rapid filling of blood into a heart that dilated

241
Q

4th heart sound

A

vigorous contraction of atria pumping into ventricle

242
Q

systolic murmur

A
  • stenosis of aortic/pulmonic valveor- insufficient/incompetent mitral/tricuspid valve
243
Q

diastolic murmer

A

-stenosis of mitral/tricuspid valveor-insufficient aortic/pulmonic valve

244
Q

physiological splitting

A

Aortic valve followed by pulmonic valve during inspiration (negative pressure caused by inspiration pulls right ventricle out, filling takes longer- negative pressure differential; more preload)

245
Q

paradoxical splitting

A

Pulmonic followed by aortic due to left bundle branch block (come closer together during inspiration)

246
Q

persistent splitting

A

right bundle branch block- becomes exaggerated with inspiration

247
Q
  • cardiac index and units- venous pressure
A
  • 2.5-4.0 (3.1)litres/min/sq m- 3-8 mm Hg
248
Q

right atrial pressureright ventricle pressure (systolic)right ventricle pressure (end-diastolic)

A

-2-5 (2)18-30 (25)-5-5 (2)

249
Q

Pulmonary artery systolic, diastolic, mean

A

18-30 (25)6-12 (10)10-20 (15)

250
Q

Pulmonary wedge pressureleft atrial pressure

A

0-12 (6)

251
Q

left ventricle- systolicleft ventricle- diastolic

A

100-140 (120)85-105 (95)

252
Q

which action potential has the longest duration?

A

cardiac ventricle (200 ms, 10x longer)

253
Q

which action potential beings and ends at -90mV?

A

skeletal muscle

254
Q

what is a space constant

A

how easily an axon can conduct electrical activity

255
Q

small axon = ___ membrane resistance= ___ internal resistance = ___ space constant = ___ conduction

A

small axon = higher membrane resistance (but overcome by the ->) = higher internal resistance= small space constant= slow conduction

256
Q

at the depolarized region, there is a ___ in membrane polarity, which causes ___ to flow

A

reversal, current

257
Q

depolarization is caused by

A

opening of of h & m** gates of sodium channels- rapid increase in Na+ channel conductance

258
Q

repolarization is caused by

A
  • delayed increase in K+ channel conductance;- inactivation of Na+ channels (closing of h gate)
259
Q

K+ channels deactivate by

A

repolarization of membrane potential

260
Q

Na+ channels deactivate by

A

positive voltage of cell (one of few positive feedback loops)

261
Q

channel properties (M & H)

A

resting- M closed, H openactivated- m open, h openinactivated- m open, h closed

262
Q

important difference between Na and K channels

A

K+ channels don’t have H gate, are inactivated by membrane repolarization

263
Q

how does a more positive resting membrane potential affect the gating of Na channels?

A

H-gates begin to close as membrane becomes more positive; results in slow conduction & muscle weakness

264
Q

absolute vs. relative refractory periods; what channel do they depend on

A
  • absolute- h-gate is closed- relative- hyperpolarization, where voltage difference is too great for another APNA CHANNELS!
265
Q

how does calcium modulate sodium channel activity?

A

Ca binds to proteins surrounding Na channel, makes environment more positive, h-gate closes, less APs

266
Q

hyperCalCemia

A

increased plasma Ca+, Na+ channels become inactive (less available), conduction slowssigns: weak reflexes

267
Q

hyperventilation

A

blow off CO2, get less H+ in blood, get less binding of Ca2+ because of increased pH, increase membrane excitabilitysigns: agitation

268
Q

hyperKalemia

A

increased plasma K+, less K+ leaks out of neuron, inside of the cell becomes more positive, h-gates close and get less APssymptoms: slow mentation, muscle weakness

269
Q

large differences in the diameter of unmyelinated axons do/don’t change conduction velocity

A

don’t

270
Q

schwann cells increase the ______ by increasing _____

A

space constant; membrane resistance

271
Q

where is the only place you see action potentials

A

nodes of ranvier

272
Q

In MS, the space constant is

A

reduced

273
Q

steps of synaptic transmission

A
  • depolarization- calcium enters- synaptic vesicles fuse via SNARE- transmitter released into synaptic cleft- NTs bind or diffuse (NO)- NTs cleared away
274
Q

two types of post-synaptic events

A

ionotropic- quick- opening of ion channelsmetabotropic- slow- GPCRs

275
Q

BoTX mechanisms, symptoms

A
  • cleaves SNAREs (synaptobrevin, SNAP-25, and syntaxin); prevents fusion of vesicles - affects peripheral cholinergic fibers - flaccid paralysis & autonomic symptoms
276
Q

TeTX mechanisms, symptoms

A
  • cleaves SNAREs (synaptobrevin); prevents fusion of vesicles - taken up by inhibitory neurons in spinal cord - spastic paralysis & death
277
Q

types of cholinergic fibers

A
  • all preganglionics - postganglionics of parasympathetic NS- basal forebrain- brainstem- NMJs
278
Q

two types of Ach receptors

A

nicotinic- fast- ionotropicmuscarinic- slow- metabotropic

279
Q

opening of ion channels (PSC) results in

A

PSP- postsynaptic potential (NOT AP)

280
Q

types of excitatory NTs

A

Ach, glutamate- inward Na, outward K= EPSC

281
Q

what is an EPSP

A

cation movement which depolarizes the cell to around ~0mv, ** increasing the probability that an action potential will be fired

282
Q

inhibitory NTs; act on which channels

A

glycine, GABA; changes permeability to Cl, moves more towards -65mV and LOCKS- will always prevent AP

283
Q

what does the ANS control

A

MOTOR SYSTEM- cardiac muscle, smooth muscle, glands- has motor efferents and visceral afferents

284
Q

function of ANS

A

homeostasis, respond to external stimuli

285
Q

major autonomic neurotransmitters

A

** Ach and norepinephrine (NE)**(epinephrine is central NT, but in ANS is mainly hormone)

286
Q

differences between neuron-neuron (and neuron-SKM) and neuron-viscera (ANS)

A
  • well defined vs en passant- little vs. great distance- ionotropic vs metabotropic - direct effect vs. direct&neuromodulatory effect
287
Q

effects of nerve gas (sarin)

A

inhibits Ache, prevent Ach degredation; have too much Ach in cholinergic synapse, overstimulate muscarinic receptors causing convulsions & paralysis

288
Q

treatment of WMD gases

A
  • diazepam: seizures- atropine: blocks Ach receptors- 2PAM (pralidoxime)- recover Ache function
289
Q

NT for adrenergic neurotransmission; how its terminated; where degrading enzymes exist

A

NE synthesized in vesicles from DOPA; MAO and COMT; degrading enzymes in cytosol, mitochondria, circulation

290
Q

location of pre-ganglionic cell bodies of sympathethic NS

A

C8lateral horn of thoracics upper lumbar

291
Q

what do preganglionic sympathetic neurons secrete

A

Ach- acts on nicotinic receptors- ionotropic, fast acting

292
Q

location of post-ganglionic cell bodies of sympathethic NS

A
  • para-vertebral (sympathetic trunk)- pre-vertebral ganglia (abdomen)
293
Q

sympathetic pre-ganglionic fibers are shorter/longer than parasympathetic preganglionic fibers

A

shorter

294
Q

preganglionic neurons are mostly ipsilateral/contralateral except for ___, which are bilateral

A

ipsilateral; pelvic viscera/intestines

295
Q

why is the adrenal medulla an exception

A

preganglionic neruons PASS THROUGH splanchnic; have NO post ganglionic neuron- is nicotinic - causes bolus release of NE/E into blood

296
Q

why are sweat glands an exception

A

they’re sympathetic, but activated by Ach NOT NE

297
Q

sympathetic post ganglionic fibers normally secrete

A

norepinephrine

298
Q

autonomic centers in brain

A

pons (breathing)medulla (blood vessels)hypothalamus (master)

299
Q

similarities between skeletal, smooth and cardiac muscle

A

all use Ca2+all require actin & myosinchemical energy comes from ATP

300
Q

smallest to largest muscle components

A

myofilament -> sarcomere -> myofibril -> myofiber

301
Q

what happens to the I, A, and H bands during contraction

A

A band (myosin) stays the sameI band (actin) shrinksH band (between actins) shrinks

302
Q

steps in EC coupling

A
  • action potential goes down t-tubule- depolarization activates DHPR- DHPR activates ryanodine receptors - ca2+ is released from SR- ca2+ initiates muscle contraction- SERCA pumps Ca2+ back into SR lumen
303
Q

ways to regulate muscle contraction

A

fire successive APs (summate)turn more/fewer fibers onbuild bigger fiberschange resting length of fibers

304
Q

sarcomeres in parallel add _____, but in series add _____

A

parallel/forceseries/shortening

305
Q

describe length-tension diagram

A

lots of stress-too short- stericsno stress- too long- no overlap

306
Q

isotonic contraction

A

muscle contracts and shortens- (includes concentric and eccentric contractions)- tension remains constant despite a change in muscle weights (bicep curls)load < tension

307
Q

isometric contraction

A

muscle contracts but does not shorten; muscle actively held at a fixed length, like when you flex to show your biceps, grip an objectload = tension

308
Q

what counts for 50-70% of all ATP consumed? where is the rest used up?

A
  • actomyosin ATPase (crossbridging)- SERCA CA2+ ATPase- Na/K ATPase
309
Q

sources of ATP for muscle metabolism

A
  • creatine phosphate- 1st used and depleated- oxidative phosphorlation - glycolysis (anerobic exercise)
310
Q

types of muscle fibers

A

type 1- slow- oxidative phosphorylation- postural muscles- lots of blood vessels/mitochondriatype 2- fast- glycolysis- fast & forceful

311
Q

difference in E-C coupling between skeletal muscle and cardiac muscle

A

DHPR physical coupling vs Ca2+ induced Ca2+ release

312
Q

weight training increases

A

the number of myofibrils

313
Q

endurance increases

A

the number of mitochondria

314
Q

relationship between alpha and beta adrenergic receptors and smooth muscle activation

A
  • alpha decreases cAMP and beta increases it- cAMP stimulates PKA to phosphorylate MLCK, resulting in RELAXATION
315
Q

relationship between nitric oxide and smooth muscle contraction

A

vagal stimulation increases Ach in blood, which binds to endothelial cells, causing them to release NO; NO increases cGMP which stimulates the MLCP, resulting in de-phosphorylation of the light chain and relaxation of blood vessels

316
Q

sequence of electical activity

A

SAAVHisBundle branchesPurkinje

317
Q

two reasons for deviation of membrane potential from Nernst equation

A

1) small sodium influx2) decrease in potassium permeability (inward rectification)

318
Q

two causes of inward rectification

A

1) chemical- decrease in extracellular K+2) electrical- depolarization of the membrane

319
Q

channels during fast action potential

A

0- fast Na channels let Na in1- transient Ito channels let K+ out2- slow calcium channels let calcium in, transient channels close, trapping K+ in3- delayed potassium channels open, letting K+ out4- K+ equilibrates (IK1’s are open)

320
Q

how hypokalemia affects resting membrane potential

A

get no net change in voltage

321
Q

how hyperkalemia affects membrane potential

A

membrane potential becomes more positive

322
Q

channels during slow AP

A

4- funny channels let more Na in than K+ out2- voltage Ca2+ channels open, and Ca2+ goes in3- K+ channels open, K+ leaves, get repolarization

323
Q

slow vs fast AP in heart

A

slow- pace maker (e.g. SA cells)fast- contractile cells

324
Q

what does TTX do?

A

block fast Na+ channels, turns contractile cells to slow conduction

325
Q

3 types of junctions found at intercalated disks

A

fascia adherinsmacular adherinsgap junctions (connexons)

326
Q

what are gap junctions sensitive to

A

Ca2+ and H+

327
Q

properties of pacemaker cells

A

function: pace makesmall diameterfew gap junctionsfew myofibrils

328
Q

properties of atrial and ventricular muscle cells

A

function: contractionmedium diameterabundant gap junctionsabundant myofibrils

329
Q

properties of His/bundle branches/Purkinjes

A

function: rapid conductionlarge diameterabundant gap junctionsfew myofibrils

330
Q

2 factors that determine cardiac conduction

A

1) space constant ((Rm/Ri)^1/2)2) rate of rise and amplitude of action potential

331
Q

membrane resistance is ___ related to K+ permeability

A

inversely

332
Q

internal resistance is ____ related to number of gap junction connections and ______ related to cell diameter

A

inversely related

333
Q

conduction is strictly related to which part of the action potential?

A

upstroke- sodium channels

334
Q

conditions that can change RMP

A

hyperkalemiapremature excitationischemia - build of of K+ in tissue

335
Q

P-R interval

A

conduction time from atrial muscle-AV node-his-purkinje- 200 ms

336
Q

QRS interval

A

conduction time from endocardial to epicardial surface- 100 ms

337
Q

AV nodal conduction abnormalities- type 1

A

abnormal prolongation in P-R interval (1:1 conduction)

338
Q

AV nodal conduction abnormalities- type 2

A

some atrial impulses fail to activate ventricles; not all P waves followed by QRS (e.g. 2:1 conudction)

339
Q

AV nodal conduction abnormalities- type 3

A

complete AV block; no consistent P-R interval

340
Q

sympathetic innervation to the heart

A
  • NE- acts on beta adrenergic receptors- increases speed of all things in the heart- increases cAMP and inward calcium
341
Q

parasympathetic innervation to the heart

A
  • Ach (vagal)- acts on muscarinic receptors - acts on everything up to AV node- increases K+ permeability
342
Q

supraventricular tachycardia

A
  • narrow QRS- normal sequence, just rapid- CO not affected- filling time decreased
343
Q

ventricular tachycardia

A
  • QRS is abnormally prolonged- impulse originates in ventricle and skips His-Purkinje; goes in circular pattern- conduction is slow - CO compromised
344
Q

atrial fibrillation

A
  • absence of P-waves (like static where they should be), R-R are irregular - non leathal
345
Q

ventricular fibrillation

A

lots of random electrical activity; is probably the end

346
Q

how to spot AV conduction abnormalities on EKG

A

look for how QRS follows p-wave

347
Q

what does digitalis inhibit and what can it cause

A
  • inhibits Na/K pump, reverses Na/Ca2+ pump- DADs by abnormally increasing intracellular Ca2+

Physiology (22 decks)

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