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Flashcards in Combined Test 1 Deck (347):
1

what determines coronary blood flow? what regulates it?

- determines: aortic pressure- regulates: metabolic activity/changes in arteriolar resistance

2

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

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

3

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

diastole

4

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

- endo to ALL

5

What compress endo/epicardium vessles?

Diastolic pressure and contraction

6

what is the relationship between blood flow and metabolic activity?

linear* increased metabolism, decreased resistance, increased blood flow

7

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

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

8

how does the heart get more oxygen?

it is flow limited- must vasodilate

9

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

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

10

which factors affect myocardial oxygen supply?

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

11

which factors create largest O2 demand?

- afterload- heart rate- contractility

12

what is ischemia, considering O2?

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)

13

what is coronary steal?

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

14

when would coronary steal present clinically?

- exercise-induced ischemia- stress testing- peripheral arterial disease

15

What happens to skeletal muscle circulation during exercise?

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

16

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?

20 active hyperemialargesttonic

17

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

adenosine

18

Skeletal muscle vasculature is primarily innervated by _____ fibers

sympathetic adrenergic

19

Ach causes ___ by acting on ___ coupled to ___

vasodilation muscarinic (on endothelials) NO production

20

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

- adrenal medulla- vasodilation - beta-2 adrenergic receptors- vasoconstriction - alpha adrenergic receptors

21

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

aerobic metabolism of glucosemost metabolically active tissue in the body

22

What is the BBB due to? What can cross?

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

23

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

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

24

what is the monroe-kellie doctrine?

brain volume + cerebral vascular volume + CSF volume= constant

25

What happens as CSF pressure rises?

- 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

26

Cerebral blood flow is very sensitive to which metabolite?

PCO2

27

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

- vasoconstriction & decreased blood flow- cerebral edema (high intracranial pressures)

28

mechanism for nitric oxide

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

29

what is the cushing response?

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

30

when does the cushing response occur?

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

31

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

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

32

Pulmonary arteries are ___ compliant than regular arteries because____

7x more; they lack smooth muscle

33

Pulmonary capillaries represent ___ of the vascular resistance

40%

34

T/F Pulmonary vessels autoregulate

F

35

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

distends; increases net effect- no change!

36

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

bottom waterfall effect

37

what happens in zone 1?

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

38

what happens in zone 2?

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

39

what happens in zone 3?

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

40

primary function of cutaneous circulation

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

41

what is apical skin?

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

42

what is nonapical skin?

- lacks AV anastomoses- innervated by sympathetic fibers- postganglionics release Ach; vasodilation

43

neural control of apical skin

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

44

neural control of nonapical skin

- sympathetic vasoconstriction (NE) - active vasodilation via cholinergic fibers via bradykinin

45

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

core body temperature; hypothalamus

46

fetal circulation pathway

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

47

valves close, pressure changes, pipes shut

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

48

difference between HbF and HbA and why?

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

49

umbilical arteryumbilical veinductus venosusductus arteriosus

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

50

what happens with skin circulation and exercise?

sympathetics want to vasoconstrictinternal metabolic heat stimulates cutaneous vasodilation

51

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

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

52

What ist he portal system?

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

53

metabolic control of splanchnic circulation

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

54

hormonal control of splanchnic circulation

cholecystokinin & neurotensin increase vasodilation

55

neural control of splanchnic circulation

- 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

56

what is postprandial hyperemia?

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

57

what is the equation for ejection fraction?

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

58

what is the ejection fraction a clinical index of?

left ventricular contractility

59

systolic heart failure

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

60

diastolic heart failure

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

61

factors that determine preload

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

62

factors that determine contractility

- sympathetic nerve activity- drugs (digitalis) - disease (infarct)

63

factors that determine afterload

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

64

venous return

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

65

central venous pool

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

66

cardiac output and what it equals

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

67

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

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

68

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

- 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

69

what happens when CVP= Pmc?

blood flow ceases- have no gradient for return

70

if you increase cardiac output, what happens?

decrease CVP, increase venous return (via pressure gradient)

71

what happens at negative CVP?

large veins collapse

72

which curve does transfusion shift?

vascular function curve - higher CO for lower pressure

73

which curve does sympathetic stimulation shift?

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

74

increase venous return by increasing peripheral venous pressure (PVP)

- increased sympathetic venoconstriction - increased skeletal leg pump - increased blood volume - cardiac contraction

75

increase venous return by decreasing central venous pressure (CVP)

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

76

how do valves change venous return?

maintain pressure gradient between peripheral and central venous pools

77

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

intersection of vascular function curve and cardiac function curve

78

which curve does heart failure shift?

- cardiac function curve- shifts down progressively - hypervolemia also shifts vascular function curve out

79

2 main things that shift venous function curve

blood volumevenous tone

80

what happens with hemmorage?

- 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

81

what is Poiseuille's law?

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

82

what is the main way in which flow is regulated?

by changing vessel radius (r^4)

83

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

- 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

84

what is the definition of a non-newtonian fluid?

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

85

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

decreases; plasma skimming

86

laminar vs turbulent blood flow

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

87

what is the reynold's # and its equation?

- propensity for turbulent blood flow- R#= (density*diameter*velocity)/(viscosity)

88

what is Bernouilli's principle and its equation?

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

89

what is the laplace relationship and its equation?

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

90

what happens with an aneurysm?

decreased velocityincreased pressureincreased radiusdecreased wall thicknessALL increase wall tension

91

example of low wall tension

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

92

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

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

93

cross sectional area and the velocity of blood flow

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

94

what holds 60% of blood volume

veins (larger cross sectional area than arteries)

95

series vs parallel resistance

-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

96

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

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

97

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

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

98

3 layers ('tunica') of arterial wall

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

99

relationship between compliance and pressure

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

100

wall thickness/diameter ratio tells you what

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

101

where are continuous capillaries found?

muscle, connective tisues

102

where are fenestrated capillaries found?

kidney, intestines

103

where are discontinuous/sinusoidal capillaries found?

liver, bone marrow, spleen

104

what is the 'windkessel'/hydraulic filtering?

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

105

relationship between compliance and pulse pressure

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

106

what is pressure pulse?

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

107

what are some specific determinants of mean arterial pressure?

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

108

primary determinants of systolic & diastolic pressure?

systolic- cardiac outputdiastolic- peripheral resistance

109

if you decrease compliance, what happens to pulse pressure?

decrease compliance, increase pulse pressure

110

increase resistance, what happens to pulse pressure?

increase diastolic pressure (and some systolic)

111

what regulates peripheral arterial resistance?

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

112

two types of ways to change arteriolar radius?

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

113

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

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

114

changes that occur during exercise

- 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

115

structures of microcirculation

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

116

characteristics of capillary blood flow

- slow- intermittent, not uniform/1 direction- follows pressure gradients

117

what is a Rouleaux formation?

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

118

pressure gradients in capillaries

hydrostatic- 32 to 15osmotic- 25

119

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

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

120

what determines capillary hydrostatic pressure?

pre and post capillary resistance to arterial and venous flow

121

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

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

122

when hydrostatic pressure is greater than osmotic pressure, you get

filtration

123

examples of vasodilators

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

124

examples of vasoconstrictors

endothelin (ET)

125

important structural features of lymphatic system

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

126

factors governing lymph flow

- amount of filtration- skeletal muscle activity- valves

127

specific causes of edema

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

128

what is edema?

excess fluid accumulation in interstitial space

129

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

- venous; excessive arterial pressure is normally dissipated by resistance

130

what is resting sympathetic tone and what is it due to

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

131

active vs passive mechanisms

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

132

two types of inputs

sympathetic adrenergic- increases resistancesympathetic cholinergic- decreases resistance

133

which type of sympathetic fibers cause active vasodilation?

sympathetic cholinergics (release Ach as opposed to Ne)

134

what are alpha-1 receptors?

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

135

what are beta-2 receptors?

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

136

baroreceptors- anatomy

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

137

baroreceptors- mechanism

- 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

138

ways sympathetics/PS change via baroreceptor

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

139

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

changes & phasic

140

what are chemoreceptors activated by?

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

141

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

less

142

what do chemoreceptors stimulate?

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

143

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

- renin-angiotensin-aldosterone- dehydration or heart failure over weeks

144

RAA pathway

- 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

local mechanisms responsible for vascular resistance

autoregulation (myogeneic, metabolic)endothelialmechanical

146

what is autoregulation? what are the two primary mechanisms?

- 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

auto-regulation among different organs

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

148

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

autoregulation

149

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

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

150

what is active hyperemia?

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

151

what is reactive hyperemia?

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

152

how does mechanical activity regulate blood flow?

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

153

where does mechanical activity regulate blood flow

muscle contraction, alveolar pressure, tumors, aortic stenosis

154

what is shock a primary reaction to?

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

155

Refractory characteristics of slow vs fast APs

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

156

R on T phenomenon- PVCs

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

what is special about the refractory period of the AV node

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

158

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

AV node refractory characteristics

159

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

Calcium channel blocker or Beta blocker

160

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

diastole

161

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

systole Q-T

162

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

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

hierarchy of cardiac pacemaker activity

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

164

diastolic depolarization- SA node

-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

diastolic depolarization- Purkinje fibers

- hyperpolarization-activated inward current of sodium (funny channels) - deactivation of K+ current

166

things that change heart rate

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

167

how would vagal nerve stimulation affect an EKG recording?

would have a longer R-R (less bpm)

168

what is sinus arrhythmia

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

169

heart rate is slower during expiration/inspiration

expiration

170

molecular reasons for cardiac arrhythmia

impulse formation, conduction, or both

171

electrical mechanisms responsible for dysrhythmias

altered automaticity, re-entry of excitation, triggered activity

172

causes of tachy-dysrhythmias

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

173

causes of brady-dysrhythmias

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

174

causes of re-entry excitations

ischemiainfarctioncongenital bypass tracts (WPW)

175

causes of DADs

"Delayed afterdepolarization" digitaliselevated catecholaminesrapid heart beatEVERYTHING TOGETHER

176

causes of EADs

"Early after depolarization" acidosis (ischemia) hypokalemiaquinidineslow heart rates

177

3 requirements for re-entry of excitation

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

178

anti-arrhythmic therapies

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

179

PR interval length

0.12-0.2 seconds

180

QRS complex length

0.07-0.1 seconds

181

QT interval length

0.25-0.43 seconds

182

cardiac E-C coupling steps (CICR)

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

structure-function EC coupling: sarcolemma

- propagates action potentials- controls Ca2+ influx via slow inward Ca2+ current

184

structure-function EC coupling: T-tubules

- transmits electrical activity to cell interior - located at Z-lines

185

structure-function EC coupling: SR, terminal cisternae

- where Ca2+ influx triggers opening of Ca2+ release channels

186

structure-function EC coupling: SR, longitudinal cisternae

- cite of Ca2+ re-uptake to initiate relaxation

187

structure-function EC coupling: troponin C

- Ca2+ receptor on actin (contractile protein)

188

cardiac vs skeletal muscle: size, connection, activation

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

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

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

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

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

191

what are catecholamines

NE (neurotransmitter) and E (hormone)

192

mechanism of catecholamines

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

193

what does PKA phosphorylate in the catecholamine cascade?

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

mechanism of calcium channel blockers

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

3 factors that change muscle contraction via a change in contractility

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

196

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

contractility

197

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

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

198

premature beat results in a ___ than normal contraction

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

what is a PESP

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

200

signs of A-fib w/ radial pulse

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

contractility of the heart is ____ with a premature beat

reduced

202

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

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

203

four factors that determine cardiac output

1) heart rate2) myocardial contractility3) preload4) afterload

204

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

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

205

afterload is any force that _____

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

206

a premature beat is a _____ contraction

isometric

207

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

stiff; heart

208

the slope of the resting tension curve is primarily determined by

muscle compliance

209

the slope of the active tension curve is primarily determined by

muscle contractility

210

what is resting diastolic tension

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

211

what is active systolic tension

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

212

stretching cardiac muscle ...

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

213

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

sympathetics; heart failure

214

an increase in preload ____ the amount of muscle shortening

increases

215

an increase in afterload ___ the amount of muscle shortening

decreases

216

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

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

217

afterload is synonymous with what

force

218

increasing afterload

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

219

at a given afterload, an increase in preload

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

220

at a given afterload, an increase in contractility

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

221

EKG inferior view of the heart

leads 2, 3 and aVF

222

EKG lateral view of the heart

leads 1, aVL, V5, V6

223

EKG anterior view of the heart

leads V3, V4

224

EKG septal view of the heart

leads V1, V2

225

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

II, down and left

226

order of ventricular depolarization

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

227

why is the vector of repolarization the same as depoarlization?

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

228

what is the last part of the heart to depolarize?

epicardial surface of the left ventricle

229

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

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

230

normal angles for Einthoven's triangle

-30* - 105*

231

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

left axis

232

how to use hexaxial reference to approximate the MFPV

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

einthoven triangle method

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

234

things that skew MFPV

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

235

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

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

236

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

hypertrophy- more cells= more current

237

phases of the cardiac cycle

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

238

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

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

239

ACV waves

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

240

3rd heart sound

rapid filling of blood into a heart that dilated

241

4th heart sound

vigorous contraction of atria pumping into ventricle

242

systolic murmur

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

243

diastolic murmer

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

244

physiological splitting

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

paradoxical splitting

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

246

persistent splitting

right bundle branch block- becomes exaggerated with inspiration

247

- cardiac index and units- venous pressure

- 2.5-4.0 (3.1)litres/min/sq m- 3-8 mm Hg

248

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

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

249

Pulmonary artery systolic, diastolic, mean

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

250

Pulmonary wedge pressureleft atrial pressure

0-12 (6)

251

left ventricle- systolicleft ventricle- diastolic

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

252

which action potential has the longest duration?

cardiac ventricle (200 ms, 10x longer)

253

which action potential beings and ends at -90mV?

skeletal muscle

254

what is a space constant

how easily an axon can conduct electrical activity

255

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

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

256

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

reversal, current

257

depolarization is caused by

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

258

repolarization is caused by

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

259

K+ channels deactivate by

repolarization of membrane potential

260

Na+ channels deactivate by

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

261

channel properties (M & H)

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

262

important difference between Na and K channels

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

263

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

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

264

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

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

265

how does calcium modulate sodium channel activity?

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

266

hyperCalCemia

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

267

hyperventilation

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

268

hyperKalemia

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

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

don't

270

schwann cells increase the ______ by increasing _____

space constant; membrane resistance

271

where is the only place you see action potentials

nodes of ranvier

272

In MS, the space constant is

reduced

273

steps of synaptic transmission

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

274

two types of post-synaptic events

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

275

BoTX mechanisms, symptoms

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

276

TeTX mechanisms, symptoms

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

277

types of cholinergic fibers

- all preganglionics - postganglionics of parasympathetic NS- basal forebrain- brainstem- NMJs

278

two types of Ach receptors

nicotinic- fast- ionotropicmuscarinic- slow- metabotropic

279

opening of ion channels (PSC) results in

PSP- postsynaptic potential (NOT AP)

280

types of excitatory NTs

Ach, glutamate- inward Na, outward K= EPSC

281

what is an EPSP

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

282

inhibitory NTs; act on which channels

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

283

what does the ANS control

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

284

function of ANS

homeostasis, respond to external stimuli

285

major autonomic neurotransmitters

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

286

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

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

287

effects of nerve gas (sarin)

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

288

treatment of WMD gases

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

289

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

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

290

location of pre-ganglionic cell bodies of sympathethic NS

C8lateral horn of thoracics upper lumbar

291

what do preganglionic sympathetic neurons secrete

Ach- acts on nicotinic receptors- ionotropic, fast acting

292

location of post-ganglionic cell bodies of sympathethic NS

- para-vertebral (sympathetic trunk)- pre-vertebral ganglia (abdomen)

293

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

shorter

294

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

ipsilateral; pelvic viscera/intestines

295

why is the adrenal medulla an exception

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

296

why are sweat glands an exception

they're sympathetic, but activated by Ach NOT NE

297

sympathetic post ganglionic fibers normally secrete

norepinephrine

298

autonomic centers in brain

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

299

similarities between skeletal, smooth and cardiac muscle

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

300

smallest to largest muscle components

myofilament -> sarcomere -> myofibril -> myofiber

301

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

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

302

steps in EC coupling

- 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

ways to regulate muscle contraction

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

304

sarcomeres in parallel add _____, but in series add _____

parallel/forceseries/shortening

305

describe length-tension diagram

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

306

isotonic contraction

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

307

isometric contraction

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

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

- actomyosin ATPase (crossbridging)- SERCA CA2+ ATPase- Na/K ATPase

309

sources of ATP for muscle metabolism

- creatine phosphate- 1st used and depleated- oxidative phosphorlation - glycolysis (anerobic exercise)

310

types of muscle fibers

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

311

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

DHPR physical coupling vs Ca2+ induced Ca2+ release

312

weight training increases

the number of myofibrils

313

endurance increases

the number of mitochondria

314

relationship between alpha and beta adrenergic receptors and smooth muscle activation

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

315

relationship between nitric oxide and smooth muscle contraction

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

sequence of electical activity

SAAVHisBundle branchesPurkinje

317

two reasons for deviation of membrane potential from Nernst equation

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

318

two causes of inward rectification

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

319

channels during fast action potential

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

how hypokalemia affects resting membrane potential

get no net change in voltage

321

how hyperkalemia affects membrane potential

membrane potential becomes more positive

322

channels during slow AP

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

slow vs fast AP in heart

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

324

what does TTX do?

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

325

3 types of junctions found at intercalated disks

fascia adherinsmacular adherinsgap junctions (connexons)

326

what are gap junctions sensitive to

Ca2+ and H+

327

properties of pacemaker cells

function: pace makesmall diameterfew gap junctionsfew myofibrils

328

properties of atrial and ventricular muscle cells

function: contractionmedium diameterabundant gap junctionsabundant myofibrils

329

properties of His/bundle branches/Purkinjes

function: rapid conductionlarge diameterabundant gap junctionsfew myofibrils

330

2 factors that determine cardiac conduction

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

331

membrane resistance is ___ related to K+ permeability

inversely

332

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

inversely related

333

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

upstroke- sodium channels

334

conditions that can change RMP

hyperkalemiapremature excitationischemia - build of of K+ in tissue

335

P-R interval

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

336

QRS interval

conduction time from endocardial to epicardial surface- 100 ms

337

AV nodal conduction abnormalities- type 1

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

338

AV nodal conduction abnormalities- type 2

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

339

AV nodal conduction abnormalities- type 3

complete AV block; no consistent P-R interval

340

sympathetic innervation to the heart

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

341

parasympathetic innervation to the heart

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

342

supraventricular tachycardia

- narrow QRS- normal sequence, just rapid- CO not affected- filling time decreased

343

ventricular tachycardia

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

344

atrial fibrillation

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

345

ventricular fibrillation

lots of random electrical activity; is probably the end

346

how to spot AV conduction abnormalities on EKG

look for how QRS follows p-wave

347

what does digitalis inhibit and what can it cause

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