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CardioPulm > Final > Flashcards

Final Flashcards

1
Q

Whats the first part of the ventricular muscle mass to depolarize during contraction

A

Interventricular septum (left to right)

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2
Q

What is the first myocardial layer to receive depolarization signal in the ventricles

A

Subendocardial

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3
Q

What do we call the “flatline” when no electrical current is being detected by the ECG leads

A

Isoelectric line

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4
Q

What creates a positive deflection on the isoelectric line of an ECG

A

Depolarization occurring toward the lead
-OR-
Repolarizing current away from the lead

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5
Q

What produces a negative deflection from the ECG isoelectric line

A

Depolarization occurring away from the lead
-OR-
Repolarizing current toward the lead

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6
Q

How much electrical charge needs to be detected in the ECG leads to produce a deflection with magnitude 10 mm

A

1 mV

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7
Q

Where. Is lead 1 placed

A

4th intercostal space on the right (just lateral to sternum)

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8
Q

Where is lead 6 placed

A

5th intercostal space on the left midaxillary line

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9
Q

What happens during p wave

A

Atrial depolarization

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10
Q

When ventricular contraction begins we see positive deflection in the reading from lead __ and negative deflection from lead __

A

1, 6 (because its moving left to right)

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11
Q

Why is. Ventricular depolarization a negative deflection from the isoelectric line for lead. 1?

A

Because it occurs so strongly in the left ventricle, it overwhelms what happens in right ventricle (from subendocardium to epicardium occurs away from lead 1)

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12
Q

What type of deflection does ventricular contraction produce in v6 lead reading

A

Positive (subendocardium to epicardium is toward that lead)

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13
Q

What part of ECG measures ventricular depolarization

A

Qrs

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14
Q

In what. Direction does ventricular repolarization occur

A

From epicardium to subendocardium

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15
Q

How does ventricular repolarization appear in V1 reading? What about V6?

A

V1: neg
V6: pos

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16
Q

What is a t wave

A

Ventricular repolarization

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17
Q

Which part of the ECG is the broadest? (Aka which part of heart contraction occurs the slowest)

A

Ventricular repolarization (t wave)

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18
Q

Qrs and t waves tend to share what relationship

A

Concordant : they go in the same direction on ECG

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19
Q

Atrial repolarization occurs when

A

During qrs complex so we don’t see it on the ECG

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20
Q

Of the atria, AV node, His-Purkinje, and ventricle who has the fastest and slowest conduction velocity?

A

slowest- his-purkinje
ventricle and atria
fastest- AV node

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21
Q

Where do you find the Na (f) gates and what’s special about them?

A

SA and AV node where it causes SLOW depolarization during rest phase

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22
Q

Ventricles, atria, and purkinje system have ____ resting potentials, ____ upstroke, and ____ duration

A

stable
rapid
long

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23
Q

In APs of ventricles, atria, purkinje system What do you call the phase with resting potential and how is it sustained?

A 
phase 4
high K (c) conductance
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24
Q

In APs of ventricles, atria, purkinje system What causes phase 0? What is phase 0?

A

rapid upstroke caused by opening of Na channels and crossing threshold

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25
Q

In APs of ventricles, atria, purkinje system What causes the small depolarization? What phase is that?

A

phase 1
Na (m) gates close
some K (a) open

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26
Q

In APs of ventricles, atria, purkinje system What sustains the plateau phase? What phase is that?

A

2

slow Ca opens and close special, voltage gated K (b) channels

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27
Q

In APs of ventricles, atria, purkinje system What phase is complete depolarization? What causes it?

A

phase 3
slow Ca channels close
special K channels open

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28
Q

Why is the SA node said to exhibit automaticity/

A

RMP gradually depolarizes until it reaches threshold and fires

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29
Q

Why doesn’t AV node dominate the pacemaking activity?

A

it gradually depolarizes too but it get stimulated by SA node’s AP before it can reach threshold on its own

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30
Q

What causes phase 0 in AV and SA nodes?

A

opening of slow Ca gates

closing of K (b) gates

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31
Q

What phases are you missing in SA and Av nodes? Why?

A

1 and 2

due to scarcity of traditional, voltage gated Na (m) channels)

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32
Q

What causes phase 3 in sa and AV nodes?

A

closing of CA gates and opening of special K (b) gates

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33
Q

What causes phase 4 in sa and AV nodes?

A

opening of special voltage na (f) gates

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34
Q

When do Na (f) gates open?

A

when membrane is repolarized

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35
Q

If both the SA and AV nodes fail who takes over pacemaking?

A

bundle of His/purkinje fibers

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36
Q

Why is there a pause before purkinje fibers take over?

A

stay polarized for a while but if not stimulated they’ll begin to spontaneously depolarize during phase 4

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37
Q

How can we make the conduction velocity faster?

A

higher inward current (Na(m)) or slow Ca

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38
Q

how will phase 0 look if we have a faster velocity?

A

steeper

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39
Q

What type of fiber allows for the faster transmission of ap and therefore velocity?

A

BIG fiber

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40
Q

Why is it beneficial for there to be a delay in the AV?

A

allows atria to empty into ventricles before ventricles contract

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41
Q

what is important to help prevent arrhythmias?

A

refractory period

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42
Q

What do we call effects that change rate of depolarization of SA node and therefore heart rate?

A

chronotropic

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43
Q

A positive chronoctropic makes the SA node depolarize…

A

faster!

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44
Q

What do we call effects that effect the speed of conduction?

A

dromotropic

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45
Q

How does the parasympathetic system slow down the heart rate? What do we call this effect

A

decreases opening of Na (f) gates during phase 4 in sa and av nodes
negative chronotropic

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46
Q

What is the neurotransmitter and receptor used by parasympathetic?

A

acetylcholine

muscarinic in heart

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47
Q

What is the receptor and neurotransmitter used by the sympathetic system to affect the heart?

A

norepinephrine

beta-1

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48
Q

How does the sympathetic system increase the heart rate? What do we call this effect?

A

increases opening of special Na (f)gates increases depolarization
positive chronotropy

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49
Q

What acts as a voltage gated Ca channel in cardiac tissue?

A

dihydropyridine (DHPR)

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50
Q

Calcium acts as a ligand for what ligand gated channel for muscle contraction?

A

ryanodine receptors (RyRs)

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51
Q

What is increased force of contraction?

A

positive inotropy

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52
Q

What is contractility of cardiac tissue proportional to?

A

amount of Ca available to troponin on the actin filaments

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53
Q

What type of an effect does sympathetic system have on heart?

A

positive inotropic

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54
Q

What does norepinephrine on beta-1 receptors cause?

A

more ca to enter interstitial spacedzring AP and also causes more CA to be sequestered in Sr

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55
Q

What does the parasympathetic innervate in the heart? What kind of an effect does it have?

A

atria and sparsely ventricles

negative inotropic effect

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56
Q

What happens with calcium when we have increased HR?

A

more Ca to accumulate and remain intracellularly (sequestered in SR) therefore more Ca released per AP so stronger contraction

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57
Q

What effect does digoxin (cardiac glycoside) have? How?

A

positive inotropic
blocks Na/K pump
intra Na increases decreasing gradient
Na/C exchanger less effective so intra Ca increases

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58
Q

What do we call the amount of wall tension in the right or left ventricle just before contraction is initiated?

A

preload

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59
Q

How does the wall tension compare between two chambers with the same chamber pressure : one is dilated and one isnt

A

dilated one has greater wall tension

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60
Q

What is the amount of chamber pressure that must be delivered to cause ejection of blood?

A

afterload

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61
Q

What is the after load a little greater than but essentially equal to?

A

pressure in aorta or pulmonary artery

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62
Q

What determines the amount of actin/myosin overlap? If this overlap is very efficient what can develop?

A

sarcomere length

greater tension when contraction is initiated

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63
Q

What is velocity of contraction inversely proportional to?

A

afterload

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64
Q

When is the velocity of contraction greatest in relation to after load?

A

when after load is 0

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65
Q

The greater the preload the more efficient the initial overlap of action and myosin causing what?

A

more forceful contraction

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66
Q

What causes greater contraction force, stroke volume, ejection fraction and cardiac output?

A

greater preload

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67
Q

Stroke volume =

A

EDV- ESV

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68
Q

Ejection fraction =

A

SV/EDV

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69
Q

Positive or negative inotropes will increase stroke volume, ejection fraction, and cardiac output?

A

positive

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70
Q

Cardiac work = work per heart beat =

A

stroke volume x aortic pressure

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71
Q

What is stroke work dependent on?

A

after load
diameter of chamber (greater = less efficient)
inotropic state

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72
Q

Minute work =

A

stroke work x heart rate

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73
Q

What are three ways to measure cardiac output? What will these show for greater cardiac output?

A

fick, thermodilution, dye

more diluted in blood

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74
Q

What do we call the technique used to measure CO by adding oxygen via lungs and measure oxygen difference before and after lungs?

A

fick

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75
Q

What do we call the way of measuring CO by adding cold fluid in pulmonary artery and measuring downstream how much it cools the blood?

A

dthemordilution

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76
Q

What do we call the way of measuring CO by adding a quantity of dye and measure how much the color change is downstream?

A

dye

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77
Q

Mean systemic is proportional to what two things?

A

blood volume

preload

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78
Q

At equilibrium cardiac output = ___?

A

venous return

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79
Q

How does increasing blood volume increase cardiac output?

A

increases preload increases cardiac output

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80
Q

Increasing total peripheral resistance does what to cardiac output

A

decreases

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81
Q

inorder for shortening to occur in muscle contraction, ca++ must bind which of the following

A

troponin

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82
Q

what attaches to the z line

A

actin

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83
Q

the A band is comprised of what

A

myosin

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84
Q

whats the major cause of phase 0 of neural action potential (depolarization)

A

increased Na+ conductance

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85
Q

what ion maintains neural resting potential

A

K+ conductance

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86
Q

whats the major cause of pass 1 (depolarization) in neural action potential

A

K+ gates open

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87
Q

4 steps of hemostasis

A

vascular spasm
form platelet plug
form blood clot
repair damage

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88
Q

what are platelets

A

cell fragments of megakaryocytes

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89
Q

we make platelets in response to what hormonal signal

A

thrombopoietin (TPO)

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90
Q

where do we make thrombopoietin?

A

liver

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91
Q

platelets, megakaryocytic, and some other hematopoietic cells contain a JAKSTAT Thrombopoeitin receptor called what

A

mpl (CD-110)

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92
Q

if thrombopoeitin binds to its receptor on a platelet what happens?

A

the platelet internalizes it and destroys it so it can’t tell megakaryocytes to make more platelet

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93
Q

mutation in TPO receptor can lead to what condition

A

polycythemia vera

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94
Q

platelets have actin and myosin which allow them to contract to perform what function

A

empty vesicles

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95
Q

what organelles remain in platelets

A

mitochondria, ER remnants to store Ca++

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96
Q

how do platelets help determine the amount of vasoconstriction/ vasodilation that occurs in vessels

A

COX1 (TxA2 leads to constriction and platelet aggregation), serotonin (vasoconstrictor)

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97
Q

what do platelets have that help them maintain stability during clot formation

A

fibrin stabilizing factor

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98
Q

how do platelets repair themselves

A

platelet derived growth factor

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99
Q

platelets have what on their membrane

A

glycoproteins (get sticky when activated), phospholipids, collagen receptors

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100
Q

what triggers EPO release? TPO release?

A

EPO- low O2 in kidney

TPO- constant release

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101
Q

how do we control EPO levels? TPO?

A

EPO- renal cells continually measure HIF accumulation

TPO- its internalized and destroyed by circulating platelets

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102
Q

what is the first thing that happens after a blood vessel is damaged

A

the smooth muscle spasms (mechanism is more effective in bigger vessels with more SM)

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103
Q

vascular spasm can occur by myogenic (injury to SM) or what other mechanism

A

platelet factor activation (serotonin and thromboxane A2)

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104
Q

what initiates formation of a platelet plug

A

break in vascular wall exposes collagen- platelets bind here

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105
Q

this guy is a plasma protein who binds between collagen and platelet receptor: part one of platelet plug formation

A

von willebrand factor

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106
Q

once the platelet is bound to the collagen exposed in a damaged vessel, the platelet “activates” what does this mean?

A

platelet swells and extends podocytes

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107
Q

after platelet activation, what occurs

A

swelling, contraction, granules leave platelet, STICKY platelets are attracted and gather at the injured area

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108
Q

platelets and fibrin that make up a clot interact to squeeze out plasma and then solidify the clot (thus closing wound) during what phase

A

clot retraction

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109
Q

what makes up the meshwork found in blood coagulation

A

fibrin and the platelets which bind it together (and RBCs)

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110
Q

how do the platelets go about forming a network with fibrin

A

they have fibrin receptors and they contract (REQUIRES CA++) to bring everything togehter

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111
Q

what do platelets release to being the repair of damage

A

platelet derived growth factor

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112
Q

what does platelet derived growth factor do

A

tells fibroblasts to differentiate into SM or whatever else is needed to close the hole

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113
Q

plasminogen is made in the liver, floats in plasma, is activated in the damaged tissue, and is inhibited by what?

A

tPA inhibitor (blood)

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114
Q

what does plasmin do when activated by TPA

A

fibrin lysis (breaks up the clot)

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115
Q

thrombin is floating around when we have tissue damage what is its purpose

A

activates protein C which activates TPA inhibitor so we can break up the clot

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116
Q

its important that we always try to limit clotting because the clotting factors are always present in the blood. what factors limit clotting?

A
  • smooth endothelial vessel lining
  • continuous blood flow
  • glycocalyx repels platelets
  • fibrin, heparin, prostacyclin, anti thrombin (anticoagulants)
  • protein c (inhibits Va and VIIIa so no more fibrin is created)
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117
Q

whats hemostasis

A

maintaining intact vessel surface and blood in a fluid, clot free condition to ensure tissue perfusion

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118
Q

in primary hemostasis we form the platelet plug by clumping and vasoconstriction, but in secondary hemostasis what happens?

A

platelets are activated, undergo conformational change, expose phospholipid rich portion of membrane (phospholipid platform)

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119
Q

whats the purpose of the phospholipid platform

A

accelerate fibrin production 1000 fold

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120
Q

the coagulation cascade (extrinsic) can be activated by binding of factor __ to tissue factor on damaged endothelial cells

A

VII

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121
Q

what are the vitamin K dependent factors of clotting cascade

A

II, VII, IX, X

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122
Q

vitamin k dependent factors can fully function after __ binds to a glutamic acid in their active sites (this curs in liver)

A

ca++

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123
Q

vitamin k deficiency can lead to what blood condition

A

decreased clotting

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124
Q

vitamin k deficiency is common in what conditions

A

liver disease, malabsorption, antibiotic therapy, breast fed newborns, infants whose mother is on anticonvulsant therapy

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125
Q

why is thrombin (factor IIa) such a key player

A

activates fibrin formation,
positive feedback to upstream clotting components,
paracrine activity causes NO, tPA, ADP, vWF, and PGI2 release

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126
Q

which factor attaches strands of fibrin together to make a 3D mesh

A

XIIIa

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127
Q

which factor of the extrinsic pathway can be activated by intrinsic pathway components IXa and Xa

A

VII

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128
Q

what does secondary hemostasis involve

A

formation fo fibrin which makes the clot stick together

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129
Q

what are the two tests used to measure coagulation

A

PT (prothrombin time)

aPTT (activated partial thromboplastin time)

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130
Q

which coagulation test can be used to discover a problem with the intrinsic or common pathway

A

aPTT

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131
Q

which coagulation test can be used to discover a problem with the extrinsic or common pathway

A

PT

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132
Q

if a patient has a normal PT and an abnormal aPTT what does this indicate about the function of their coagulation system?

A

issue is with intrinsic pathway

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133
Q

what do we use in the lab to anti coagulate a blood sample so that we can loo at plasma only

A

agent that chelates Ca++ (such as sodium citrate)

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134
Q

which factors need to be individually analyzed for an abnormal aPTT test

A

(intrinsic&common) 8, 9, 11, 12, 10, 5, 2, 1

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135
Q

what is an anticoagulant therapy that inhibits factors IIa, IX, and Xa

A

heparin

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136
Q

what condition has been discovered to include a deficiency of factor VIII

A

hemophilia A

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137
Q

what condition has been discovered to include a deficiency of factor IX

A

hemophilia B

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138
Q

what lab test would we use to test coagulation in heparin therapy patients

A

aPTT

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139
Q

which factors need to be individually analyzed for an abnormal PT test (abnormal if clot time >13 seconds)

A

VII, X, V, II, I

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140
Q

what type of anticoagulant therapy inhibits vitamin k thus inhibiting II, VII, IX, and X

A

coumadin (warfarin)

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141
Q

what can cause coagulation factor deficiency

A

liver disease, wash out (after hemorrhage), disseminated intravascular coagulation, inherited deficiency

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142
Q

What is the first to depolarize and thus considered the pacemaker of the heart

A

SA node

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143
Q

depolarization of the SA node causes what two results to simultaneously happen

A

atrial depolarization, AP travels in intermodal pathway to AV node

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144
Q

What ECG wave occurs when Na+ influx occurs in atrial myocytes

A

P

145
Q

AV conduction is slow causing a pause between atria and ventricle depolarization: how do we measure this on ECG

A

PR interval

146
Q

Describe. The path of depolarization in the ventricles

A

Septum first then free walls of ventricles from apex up

147
Q

Contraction of heart

A

Systole

148
Q

Relaxation of heart

A

Diastole

149
Q

Why does atrial pressure increase during ventricular systole

A

Blood continues to flow into atria via veins even though AV valves are closed

150
Q

What is. Occurring anatomically when the pressure curves of atrium and ventricle cross

A

AV valve opens or closes

151
Q

The first heart sound (luv) is. Associated with what anatomic change in heart

A

AV valve closure (when Ventricle pressure Exceeds atrial)

152
Q

What is occurring during the QRS. Wave of an ECG

A

Isovolumetric contraction of ventricle

153
Q

What pressure does L ventricle need to reach before valves open? R ventricle?

A

Diastolic pressure must be reached
L- 70
R- 15

154
Q

What do we call the point on the aortic pressure wave (mirrored also in atrial pressure curve) when the aortic valve closes

A

Dicrotic notch

155
Q

What creates the second heart sound (dub)

A

Closing aortic and pulmonary valves

156
Q

After closure of aortic and pulmonary valves, we see a major decrease in ventricular pressure that is associated with what action

A

Isovolumetric relaxation of ventricle

157
Q

What creates the third heart. Sound (normal in children, may be heard in adults)

A

Blood rushing into ventricle after opening of AV valve

158
Q

Why does aortic pressure slowly drop after ventricular contraction?

A

Blood flows into small peripheral vessels (rate is determined by resistance)

159
Q

In congenital heart failure patients, it is important to check for what peripheral blood vessel abnormality

A

Jugular venous distension

160
Q

When/ why does jugular pressure increase during atrial contraction (called the “a wave” on jugular pressure curve)

A

No valve between atria and superior vena cava means pressure is reflected into jugular during atrial contraction

161
Q

What is the “c wave” of jugular pressure (occurring after the “a wave” indicating?

A

Isovolumetric contraction of ventricles (increases pressure in atria and thus jugular vein as well)

162
Q

The final notable feature of jugular pressure graph is a slow increase in pressure called the “v wave” what is happening in the heart at this time?

A

Blood returns to atrium at this time but cannot yet enter ventricle (AV valve still closed)

163
Q

What is the fourth heart sound (normal in children but not adults)

A

Atrial contraction (last bit of blood is being squeezed into ventricle)

164
Q

If blood is moving in a direction where it shouldn’t or having a hard time moving in the correct direction: what do we hear

A

Murmur

165
Q

A murmur heard after S2 indicates backflow of blood in what area

A

Aortic or pulmonary valve backflow

166
Q

A murmur heard after S1 (diastole murmur) indicates backflow of blood in what area

A

AV valve (likely mitral valve stenosis)

167
Q

term: formation of new vascular channels by assembly of individual cell precursors called angioblasts which are derived from mesoderm (week 3)

A

vasculogenesis

168
Q

term: development of blood vessels from pre-existing vessels

A

angiogenesis

169
Q

which vessels in our body are created by vasculogenesis

A

dorsal aorta, cardinal veins

170
Q

what happens to the paired dorsal aortae in week 4

A

fuse to become abdominal aorta

171
Q

these primitive arteries are derived from splanchnic layer of lateral plate mesoderm and endoderm and eventually become celiac a, superior mesenteric a, and inferior mesenteric a

A

ventral segmental aa

172
Q

these primitive arteries are derived from intermediate mesoderm and eventually become renal and gonadal arteries

A

lateral segmental aa

173
Q

these primitive arteries supply derivatives of the somites and eventually become posterior intercostal, lumbar, and vertebral arteries

A

dorsal segmental arteries

174
Q

when do we complete the aortic arches to give off branches that enter developing head

A

end of wk 5 into 6 (day 32-37)

175
Q

artery derivatives of 1st aortic arch

A

external carotid and maxillary a

176
Q

artery derivatives of 2nd aortic arch

A

stapedial artery

177
Q

artery derivatives of 3rd aortic arch

A

common carotid and internal carotid aa

178
Q

artery derivatives of 4th aortic arch

A

left: medial aortic arch
right: proximal R subclavian a

179
Q

artery derivatives of aortic sac

A

brachiocephalic a, base of arch of aorta

180
Q

artery derivatives of 6th aortic arch

A

pulmonary arteries (Left: ductus arteriosus)

181
Q

what eventually becomes the distal part of R subclavian a and the entire L subclavian a

A

7th intersegmental a

182
Q

the ductus arterioles in a developing fetus allows baby’s circulation to skip over what part of adult circulation

A

bypass R atrium (and thus lungs)

183
Q

aeration of the lungs at birth decreases pulmonary vascular resistance and encourages blood flow to lungs and thinning of walls of pulmonary arteries. at this time what happens in the heart?

A

closure of foramen oval

184
Q

aeration of the lungs at birth decreases pulmonary vascular resistance and encourages blood flow to lungs and thinning of walls of pulmonary arteries. at this time what happens in the liver?

A

sphincter of ductus venous constricts until occluding it (this used to bring in mom’s blood from umbilicus)

185
Q

when and why does ductus arteriosus close ? (to become ligamentum arteriosum)

A

after the first breath, O2 levels increase and cause bradykinin release in lungs. smooth muscle in ductus arterioles constricts until it closes.

186
Q

a persistent ductus arteriosus causes what in newborn babies

A

left to right shunt (acyanotic)

187
Q

abnormal narrowing of the aorta is called ___ and can happen in what two places?

A

coarctation

can be pre ductal or post ductal

188
Q

what is the clinical presentation of coarctation of the aorta

A

hypertension in upper extremities, hypotension in lower extremities

189
Q

why can it be problematic to have a persistent right dorsal aorta

A

forms ring around trachea and esophagus

190
Q

what symptoms present for someone with a double aortic arch

A

stridor, respiratory infections or distress, wheezing, cough, dysphagia, vomitting

191
Q

sometimes the right subclavian artery arises from distal part of 7th intersegmental artery and this is a problem because

A

it passes behind esophagus and trachea (could be occluded)

192
Q

if you develop a right aortic arch, your trachea and esophagus may be occluded in a small space between aortic arch, pulmonary trunk, and what other structure

A

ligamentum arteriosum

193
Q

when does remodeling of inflow to the heart occur

A

wk 4-8

194
Q

whats the name of the vein that carries blood from yolk sac to the liver of the developing fetus

A

vitelline duct

195
Q

how does a developing fetus get oxygenated blood

A

from mom via umbilical vein

196
Q

what are the 3 most primitive veins in the developing fetus

A

cardinal veins (anterior, posterior, common)

197
Q

what do vitelline veins become

A

right hepatic vein, portal vein (gut to liver)

198
Q

what do umbilical veins become

A

right- degenerates

left- ductus venous within liver

199
Q

what do cardinal veins become

A

anterior- internal jugular, SVC, L brachiocephalic
posterior- root of azygos and common iliac
common- coronary sinus, contributes to SVC

200
Q

persistence of left anterior cardinal vein and failure of left brachiocephalic vein to form results in what venous system defect

A

double superior vena cava

201
Q

what embryonic vein contributes to the hepatic segment of the IVC

A

R vitelline and hepatic veins

202
Q

what embryonic vein contributes to the prerenal segment of the IVC

A

R subcardinal

203
Q

what embryonic vein contributes to the renal segment of the IVC

A

subcardinal - supracardinal anastemosis

204
Q

what embryonic vein contributes to the postrenal segment of the IVC

A

R supracardinal v

205
Q

Sinus bradycardia corresponds to. What HR

A

Less than 60 beats/// minute

206
Q

Sinus bradycardia most often results from excess ___ stimulation

A

Parasympathetic

207
Q

Who often has sinus bradycardia

A

Conditioned athletes at rest

208
Q

Extreme bradycardia may reduce blood flow to the brain causing loss of consciousness. What s the term for this

A

Syncope

209
Q

Excersize produces sympathetic stimulation to the SA node which commonly causes

A

Sinus tachycardia (greater than 100 beats/ min)

210
Q

What do you call areas in the heart that are capable of pacing in emergent situations

A

Automaticity foci

211
Q

What are the automaticity foci in the heart (they function if the SA node gives up)

A

Atrial conduction system, distal portion of AV node, purkinje fibers, bundle of his, bundle branches

212
Q

Automaticity centers express. This characteristic. Which. Means that the rapid activity suppresses slower activity

A

Overdrive suppression

213
Q

What do we call it when sympathetics slightly increase HR based on phases of respiration

A

Sinus arrhythmia (not a true arrhythmia)

214
Q

Whats the name of the part of the atrial conduction system that supplies the left atrium

A

Bachmann’s bundle

215
Q

normal pace of the ventricular automaticity foci

A

20-40 beats per minute

216
Q

when would a ventricular automaticity foci control heart rate

A

only if all pacemaking centers above failed OR complete conduction block below AV node (prevents pacing stimulus from reaching ventricles)

217
Q

if the SA node fails to pace the heart rate, what is the order in which automaticity centers take over pacemaking and what are their inherent rates

A

atrial 60-80
AV junctional 40-60
ventricular 20-40

218
Q

the P wave is upright in the readings from which ECG leads

A

1, 2, V4-V6, AVF

219
Q

the P wave is inverted in the readings from which ECG leads

A

AVR

220
Q

the P wave is variable (sometimes absent) in the readings from which ECG leads

A

3, AVL

221
Q

PR interval is time between SA node to ventricular muscle fiber firing : normal PR interval time

A

0.12 to 0.2 seconds (3-5 tiny boxes)

222
Q

short PR interval indicates what kind of arrhythmia

A

pre-excitation syndrome or nodal rhythms

223
Q

prolonged PR interval indicates what kind of arrhythmia

A

AV conduction disease

224
Q

a prolonged QRS complex indicates what kind of abnormality

A

bundle branch block, hypertrophy

225
Q

if there are no Q waves in leads V5 or V6 then we have what abnormality

A

left bundle branch block

226
Q

whats normal duration for QRS complex

A

0.05 to 0.1 seconds (1-3 tiny boxes)

227
Q

the ST segment should be found where in relation to baseline of ECG

A

isoelectric or a little elevated is normal

it should NEVER normally be depressed

228
Q

if the patients ST segment is elevated above baseline and/ or they are experiencing chest pain what do we call it

A

subepicardial injury / ischemia / infarction until proven otherwise (can be normal)

229
Q

if the patients ST segment is depressed below baseline what do we call it

A

subendocardial injury

230
Q

the T wave (ventricular repolarization) is upright in the readings from which leads

A

1, 2, V3-V6

231
Q

the T wave (ventricular repolarization) is inverted in the readings from which leads

A

AVR

232
Q

what is a normal amplitude for the T wave on an ECG reading

A

5 mm maximum- standard leads

10 mm max- precordial leads

233
Q

QT duration is the length of what action of the heart

A

ventricular systole

234
Q

the T wave is not normally depressed or inverted but if it is what should we expect

A

ischemic injury

235
Q

we can expect tall pointy T waves in what patients

A

athletes, hyperkalemia

236
Q

whats the ECG indicator for necrosis or infarction

A

Q wave or QS complex elongation

237
Q

normally the QT interval is how long?

A

less than 50% R-R segment

238
Q

how does hypokalemia show up on ECG

A

low T wave and U wave is present

239
Q

how do we know patient has left atrial enlargement? (in the condition p mitrale)

A

notched p wave (looks like an m) - leads 1-2

240
Q

how do we know a patient has p pulmonale? (right atrial enlargement)

A

tall pointy p waves in leads 2, 3, and AVF

241
Q

how can we identify AV junctional rhythm aside from counting the rate of ECG

A

inverted P waves in leads 2 and 3 (and short PR interval)

242
Q

prolonged PR interval means what

A

AV block

243
Q

shortened PR interval means what

A

AV junctional rhythm, wolff-Parkinson-White syndrome, Lown-ganong-levine syndrome

244
Q

whats treatment for sinus tachycardia (HR >100)

A

TREAT THE CAUSE- labor, anxiety, pneumonia, whatever

245
Q

if we see rhythms in addition to waves PQRST then what should be included in the differential

A

ectopic atrial rhythm, multifocal atrial tachycardia, wandering atrial pacemaker

246
Q

if we see no P waves then what should be included in the differential

A

A fib, A flutter, junctional or ventricular escape rhythms, junctional tachycardia, VT

247
Q

if we see inverted P waves after the QRS complex then what should be included in the differential

A

SVT (AV nodal re-entry tachycardia)

junctional rhythm

248
Q

How easy it is to cause a vessel to expand in response to change in lumen hydrostatic pressure

A

Compliance

249
Q

Equation for compliance

A

Change in vol/ change in pressure

250
Q

What type of vessel has the most compliance

A

Veins

251
Q

Smooth muscle contraction in veins decreases compliance making it harder to expand. Where does the blood go in this case?

A

To arteries (increasing pressure)

252
Q

The largest pressure drop in the circulatory system occurs where?

A

Arterioles

253
Q

Largest pressure reached in a large artery is reported as

A

Systolic pressure (120)

254
Q

Lowest pressure reached in large arteries is reported as

A

Diastolic pressure (80)

255
Q

How do you calculate pulse pressure

A

Systolic - diastolic pressure (120-80=40)

256
Q

How do you calculate mean pressure

A

Diastolic + 1/3 pulse pressure = 80 + (40/3) = 93.3

257
Q

What. Happens to pulse pressure when compliance decreases

A

Increase in pulse pressure

258
Q

What would increase in stroke volume do to pulse pressure

A

Increase

259
Q

What would increase in resistance do to pulse pressure

A

No change (compliance stays the same with increased resistance)

260
Q

What exactly is an ECG measuring?

A

extracellular potential

261
Q

when is the only time an ECG will cause a deflection?

A

there is a different membrane potential at part of the heart compared to the rest
current is flowing

262
Q

The ECG will not cause a deflection if there is a difference in potentials where? Why?

A

just between atria and ventricles

no current flowing between them

263
Q

At rest the extracellular potential in the heart is?

A

+90mv

264
Q

During phase 2 the extracellular potential is?

A

-15mv

265
Q

The delay in signal due to the AV node is what on the ECG?

A

PR interval

266
Q

Phase 2 causes a delay in the action potential on the ECG which we call?

A

ST segment

267
Q

The right ventricle depolarizes before the left ventricle. Which repolarizes first and why?

A

left ventricle

shorter AP

268
Q

Which phase of the action potential in the atrial muscle is represented by the P wave?

A

phase 0

269
Q

Which phase of the AP in the ventricular muscle is represented by QRS complex?

A

phase 0

270
Q

What phase of the AP in the ventricular muscle is represented by the T wave?

A

phase 3

repolarization

271
Q

Where are the K+ goes closed in the atria on the ECG?

A

p wave

272
Q

When is the Na+ most permeable in atrium on the ECG?

A

initial depolarization so p wave

273
Q

When is Na+ most permeable in the ventricles on the ECG?

A

QRS

274
Q

Segments represent what? Intervals represent what?

A

segment- single event

interval- several events

275
Q

What is the end of atrial depolarization until beginning of ventricular depolarization on ECG?

A

PR segment

276
Q

What is the end of the ventricular depolarization until beginning for ventricular repolarization on the ECG?

A

ST segment

277
Q

What is the beginning of the atrial depolarization until the beginning of the ventricular depolarization?

A

PR interval

278
Q

What is the beginning of the ventricular depolarization until the end of ventricular repolarization?

A

QT interval

279
Q

Time between dark lines on ECG is? Light lines?

A

.2 sec

.04 sec

280
Q

What is the grounding electrode? it is NOT recording!

A

RL

281
Q

What are the three standard limb leads used?

A

1: RA to LA
2: RA to LL
3: LA to LL

282
Q

What are the three augmented limb leads?

A

aVF: RA+LA to LL
aVR: LL+LA to RA
aVL: LL+RA to LA

283
Q

What leads do we look at to evaluate the inferior region of the heart?

A

II, III, aVF

284
Q

What leads do we look at to evaluate the septal region of the heart?

A

V1, V2

285
Q

What leads do we look at to evaluate the anterior region of the heart?

A

V2, V3, V4

286
Q

What leads do we look at to evaluate the lateral region of the heart?

A

I, aVL, V4-6

287
Q

What does the mean electrical axis represent? What leads do we look at to evaluate it?

A

mean electrical axis

I and aVF

288
Q

If both I and aVF are positive what do we say about the mean electrical axis?

A

normal

289
Q

If I is negative what do we say about mean electrical axis? What causes this?

A

right axis deviation

right ventricular hypertrophy

290
Q

If I is positive and aVF is negative what do we say about the mean electrical axis? What causes this?

A

left axis deviation

left ventricular hypertrophy

291
Q

What is the relationship of electrical event to mechanical event?

A

electrical event before mechanical

so ECG is ahead of mechanical events

292
Q

If the AP is extra slow getting through the AV node what will the ECG show?

A

prolonged PR interval

293
Q

If there is an ectopic pacemaker in the atrium what will the QRS and QT interval look like?

A

NORMAL

294
Q

What gates are open for the QRS segment?

A

sodium gates

295
Q

What gates are open for the ST segment?

A

calcium

296
Q

Sympathetic nervous system innervates what part of the heart?

A

BOTH atrium and ventricles

297
Q

which vessels contain the highest volume

A

veins (lowest pressure)

298
Q

which vessels contain the most area

A

capillaries

299
Q

how can we calculate velocity of blood flow

A

V=Q/A

perfusion/area

300
Q

at rest, which body systems receive the largest percentage of blood flow? (25% each)

A

renal
GI
skeletal muscle

301
Q

how do we calculate flow through a vessel

A

Q= change in pressure / resistance

302
Q

how do we calculate cardiac output

A

CO = BP / TPR(total peripheral resistance)

303
Q

how do we calculate resistance

A

R= (8viscositylength of vessel) / (pi*radius^4)

304
Q

whats the easiest way to change vascular resistance

A

change radius of the vessel

305
Q

how does resistance change if we add vasculature in series

A

add resistances for a total (increases total R when you add in series)

306
Q

how does resistance change if we add vasculature in parallel

A

decreases total resistance (like with pregnancy)

307
Q

flow becomes ___ with high velocity, large area, low viscosity

A

turbulent

308
Q

whats the equation used to predict when turbulence will occur (reynolds number)

A

[density * diameter * velocity / viscosity] = turbulent if over 2000

309
Q

what do we hear upon auscultation when turbulent flow is present

A

bruits

310
Q

what occurs in the vasculature when turbulent flow is present

A

arteriosclerosis

311
Q

what angle is lead II at?

A

60

312
Q

what angle is lead III at?

A

120

313
Q

what angle is lead I at?

A

0

314
Q

what angle is lead avF at?

A

90

315
Q

What are two ways that an antagonist works?

A
  • binds receptor but doesn’t activate it so agonist can’t

- suppress basal signaling of receptors that are constitutively active

316
Q

What do we call drugs that mimic ACh? What affect do they have on AChR?

A

cholinomimemtic agents

agonists

317
Q

What do affect do cholinoceptor-blocking drugs have on AChR?

A

antagonists

318
Q

What do we call drugs that mimic or enhance a and B receptor stimulation? Are they antagonists or agonists?

A

sympathomimetic agents

agonists

319
Q

What effects does the sympathetic system have on the SA node and atria? on what receptors does it act?

A

SA node: increase heart rate, B1>B2

atria: increase contractility and conduction velocity, B1>B2

320
Q

What effects does the parasympathetic system have on the SA node and atria? What receptors does it work on?

A

atria: decrease in contractility, M2»M3

SA node: decrease in heart rate M2»M3

321
Q

What nervous system uses dopamine?

A

sympathetic

322
Q

What nervous system controls sweat glands with what neurotransmitter and receptors?

A

sympathetic
ach
muscarinic

323
Q

What is the MAJOR neurotransmitter of the sympathetic nervous system?

A

norepinephrine

324
Q

Where does synthesis of epinephrine occur?

A

adrenal medulla

few neuronal pathways in brainstem

325
Q

What is dopamine the precursor of? Where does it act?

A

NE and epic

acts on CNS and renal vascular smooth muscle

326
Q

What are the functions of the nAChR and mAChR?

A

n- excitatory, release of catecholamines (in adrenal medulla)
m- excitatory and inhibitory

327
Q

The cholinergic receptors M1, M3, M5 are associated with what G protein? What do they result in?

A

Gq-> activation of PLC: IP3 and DAG cascade

smooth muscle contraction

328
Q

Cholinergic receptors M2 and M4 are associated with what G protein? What do they result in?

A

Gi/o inhibition of AC: decreased cAMP production so decrease in contractility

329
Q

Where do we find M2?

A

heart, nerves, smooth muscle

330
Q

Where does the synthesis of dopamine from tyrosine occur?

A

nerve cytoplasm

331
Q

Where does the conversion of dopamine to nor then epic occur?

A

vesicle

332
Q

Where does the conversion of norepi to epic mainly occur?

A

in vesicles in adrenal medulla

333
Q

The tyrosine transporter transports tyrosine into the cell. What ion is it dependent on?

A

Na

334
Q

What is the function of the vesicular monoamine transporter (VMAT-2)?

A

transports NE, epic, DA, and serotonin into vesicles

335
Q

What is the function of NE transporter (NET)?

A

imports NE into nerve terminal

336
Q

What is the effect of cocaine one neurons?

A

increases concentration of catecholamines in the synapse by blocking NET

337
Q

What is the major way of termination of catecholamine signaling?

A

reuptake via NET or DAT

then storage in VMAT-2

338
Q

What are the two main enzymes that metabolize catecholamines?

A 
monoamine oxidase (MAO)
catechol-O-methyltransferase (COMT)
339
Q

Where doe we find a1 receptors? what does activation of them cause?

A 
smooth muscle (around vasculature)
constriction
340
Q

Where do we find B2 receptors? What do they cause?

A

smooth muscle

relaxation

341
Q

Where do we find B1 receptors? What do they cause?

A

heart

increase HR and contractility

342
Q

What effect do muscarinic receptors have when activated on smooth muscle?

A

contract

don’t always cause vasoconstriction like a1

343
Q

Ach and muscarinic agonists given IV will cause vasodilation. Why?

A

release of NO

344
Q

What nervous systems does not innervate smooth muscles on blood vessels? What receptors will you not find there?

A

parasympathetic

mAChRs nor nAChRs

345
Q

Blood vessels relax in response to parasympathetic releasing ACh as long as the endothelium is intact. Why?

A

mAChRs on endothelial cells cause production and release of NO

346
Q

The release of what NT causes adrenal medulla to release epi and norepi?

A

ACh from preganglionic fibers

347
Q

What kind of receptor is found on adrenal medulla?

A

nAChR

348
Q

how do we know when we have a left axis deviation (0 to -90)

A

+ read in lead I

- read in lead AVF

349
Q

how do we know when we have right axis deviation (90 to 180)

A
  • read in lead I

+ read in lead AVF

350
Q

how do we treat sinus tachycardia

A

treat the CAUSE

351
Q

which automaticity foci in the heart serves as an O2 sensor: meaning it will fire spontaneously under hypoxic conditions

A

ventricular foci

352
Q

consuming what can lead to premature atrial contraction

A

alcohol, tobacco, COPD, and CAD in people without heart disease

353
Q

what stimulus can lead to premature ventricular contraction

A

hypoxia, nicotine, thyroid, aminophylline, digitalis, intoxication, electrolyte disorder

354
Q

at what point do premature ventricular contractions become ventricular tachycardia

A

lasts more than 30 seconds

355
Q

jugular vein distension indicates problems with which side of the heart

A

right side

356
Q

if there is an absence of p waves, we assume what condition unless proven otherwise

A

atrial fibrillation (can appear as undulating baseline up to 600 per minute)

357
Q

why do we have to worry about embolism in patients with atrial fibrillation

A

blood remains in atrium and can clot: pieces break off and emboli occur

358
Q

what causes ventricular tachycardia

A

irritable ventricular foci that decides to pace quickly

359
Q

what condition is occurring in the heart when both PAT (premature atrial tachycardia) and PJT (premature junctional tachycardia) are taking place

A

paroxysmal supraventricular tachycardia

CardioPulm (6 decks)

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