Exam 4 Flashcards

1
Q

What connects the left Atrium to the SA node & its function?

A

The Interatrial pathway (Bachman’s Bundle) & to facilitate coordinated electrical action potentials.

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2
Q

What sends the signal from the SA node to AV node?

A

The 3 internodal pathways (anterior, middle & posterior).

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3
Q

What does Isotonic contraction refer to?

A

Looking at contractions using the same weight but with different stimuli intensity or rate.

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4
Q

What is basal tension?

A

A muscle at rest without contraction.

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5
Q

What is an isometric contraction?

A

A contraction, in which the overall muscle length does not change.

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6
Q

What are iK+ ATP channels & where are they found?

A

Channels that open in response to low ATP or ischemia to reduce metabolic rate. They are found in nodal and ventricular tissue.

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7
Q

What effect do beta adrenergists have on HCN channels?

A

They facilitate wider opening of the channels, which results in a faster signal propagation from rest to threshold= faster HR.

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8
Q

How long does it take the signal to travel to the Bundle branches once the AV node receives the signal?

A

0.13seconds. (AV node receives the signal at 0.03 seconds and the L & R Bundle branches receive the signal at 0.16 seconds).

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9
Q

Through what tissue does the Bundle of His penetrate?

A

The Atrioventricular fibrous tissue

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10
Q

What is the last part to receive the action potential signal & how long does it take starting from the bundle branches?

A

It is the superior left lateral part of the left ventricle & it takes 0.06 seconds.

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11
Q

What causes the signal delay from the atria to ventricles (2 reasons)?

A

There are fewer gap junctions in the AV node & the penetrating part of the Bundle of His are smaller in diameter.

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12
Q

What is the difference of Purkinjie cells compared to Atria cells?

A

Purkinjie cells are wider & have lots of gap junctions

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13
Q

How long does the signal travel from SA to AV node?

A

0.03 seconds

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14
Q

How long does it take the for the last part of the Atria to see the electrical signal?

A

It takes 0.09 seconds

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15
Q

How long does it take the electrical signal to spread throughout the right Atrium?

A

0.07sec

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16
Q

What would cause a divided or biphasic P-wave?

A

Most likely a dilated left Atrium. Could be fibrosis or scar tissue of Bachman’s Bundle.

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17
Q

What would cause a larger P-wave?

A

Right Atrium hypertrophy

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18
Q

How long is the AV node delay?

A

0.09 sec

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19
Q

What is the combined total delay in the Bundle of His?

A

0.04sec

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20
Q

When does the conduction signal reach the Bundle branches?

A

0.16

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21
Q

What relates to the PR interval?

A

Signal travel from SA node to the Bundle branches

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22
Q

Where is the QRS initiated?

A

At the Bundle branches. The left bundle branch fires first, which reflects as the Q-wave.

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23
Q

What is indicative of a QS wave & where would one see it?

A

Indicative of ischemia & seen in Lead II

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24
Q

How long does it take for the entire depolarization to occur?

A

0.22sec

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25
Q

What prevents electrical signal travel between Atria & ventricles?

A

Cartilaginous rings

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26
Q

How does WPW present on an EKG?

A

Shortened PR interval or absorbed PR into QRS & widened QRS.

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27
Q

What are the clinical symptoms of Wolff Parkinson White?

A

Tachycardia, arrhythmias, EKG changes

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28
Q

What are accessory pathways & where are they found?

A

Abnormal pathways between atria and ventricles on the lateral aspects of the heart, they are called Bundle of Kent. Type-A is found between the Left atria & ventricle. Type-B is found between the Right atria & ventricle.

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29
Q

What is the normal Magnitude of a QRS complex?

A

1.5 – 2.0 mV

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30
Q

What would be causes of reduced voltage changes on an EKG?

A

Soft tissue, adipose tissue, air in lungs, COPD

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31
Q

When would we see the highest reading on a current meter?

A

When half of the tissue is depolarized & half is reset.

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32
Q

Where does Bachmann’s Bundle branch off?

A

Off the anterior intranodal pathway close to the SA node.

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33
Q

What are two reasons for a prolonged P wave?

A

Fibrosis/scar tissue of or around Bachmann’s Bundle & a dilated left atrium.

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34
Q

What is indicative of a peaked P wave?

A

Hypertrophy of the right atrium.

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35
Q

Which arrhythmia has circular conduction in the atria?

A

A-flutter

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36
Q

What is the difference between purkinjie cells & internodal pathways?

A

Purkinjie cells don’t have much actin & myosin & have lots of gap junctions & are wider to conduct very quickly.

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37
Q

What are the 3 LV fascicles?

A

Posterior (comes off early of the LBB), left lateral wall, & anterior fascicle (towards apex)

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38
Q

What is indicative of a QS wave is observed in Lead II?

A

Dead heart tissue.

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39
Q

How long is a perfect QT interval?

A

0.35sec

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40
Q

What is the ST segment, how long is it, & what are two other names for it?

A

All of the ventricle tissues are depolarized. It is 0.16sec, & it is also called the J-Point or Isoelectric point.

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41
Q

True or false? Infarcted tissue can reset but not depolarize.

A

False, it can depolarize but not reset.

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42
Q

On a standard 3 lead EKG which lead is least likely to have a Q wave?

A

Lead III

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43
Q

Which leads are used to check for ventricular hypertrophy & what is the amplitude?

A

Leads I, II, III & >2mV.

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44
Q

At what rate does EKG paper print & what does each individual horizontal box mean?

A

It prints at 25mm/sec. Each box is 1mm & 0.04sec.

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45
Q

How long is the RR interval supposed to be & what can it be used for?

A

0.83sec & it can be used to calculate the HR (60/RR interval= HR)

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46
Q

Where should leads V1 & V2 be placed?

A

In the 4th intercostal spaces

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47
Q

Where should lead V4 be placed?

A

In the midclavicular line/ the 5th intercostal space

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48
Q

Where should V6 be placed?

A

In line with the lateral portion of the clavicle. Also called Mid-axillary line.

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49
Q

Where should V5 be placed?

A

At the anterior axillary line

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50
Q

What are the reasons for left axis deviation?

A

Obesity, LV hypertrophy, loss of electrical activity in right side, LBBB, systemic HTN, AS, AR, age, deep exhalation, low lung volume (paralytics), lying down.

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51
Q

What are the causes for right axis deviation?

A

COPD, RV hypertrophy, RBBB, being skinny, deep inspiration, pulmonic valve stenosis, pulmonary HTN

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52
Q

What leads are used to evaluate axis deviation?

A

Lead I & III

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53
Q

What are the values for left axis deviation?

A

Anything less than +59 to -90 degrees.

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54
Q

What are the values for right axis deviation?

A

Anything greater than +59 to +180 degrees.

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55
Q

When is axis deviation considered extreme?

A

> +180 degrees.

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56
Q

The tallest normal T wave should be seen in what lead?

A

In Lead II

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57
Q

At what point do the contracted ventricles start to loosen?

A

Shortly after the end of the T-wave. (slide 12, lecture 12)

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58
Q

At what 3 points is no potential recorded?

A

When the ventricular muscle is either completely depolarized or repolarized or when current is moving perpendicular to the lead.

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59
Q

What is the mean electrical axis & what is it derived from?

A

+59 degrees & averaging out all currents.

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60
Q

Where does ventricular depolarization start?

A

At the septum & the endocardial surfaces.

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61
Q

What is Eindhoven’s law state?

A

The electrical potential of any limb equals the sum of the other two.

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62
Q

What are the Precordial leads?

A

V1 – V6

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63
Q

Which lead in a 12 Lead EKG will have the highest QRS complex?

A

V4

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64
Q

Where are the positive electrodes for aVR, aVL, & aVF located?

A

aVR= right arm, aVL= left arm, aVF= left foot

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65
Q

What are the axis of Lead I, II, & III?

A

0, 60, & 120 degrees

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66
Q

What gives us the S wave?

A

The last part to depolarize is the left lateral part of the LV, so the current flows towards the negative part of Lead III & partially towards the negative part of Lead II.

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67
Q

Should we see an S wave in Lead I & why?

A

No, current flows towards Lead I at that part of depolarization & therefore we should still see a positive deflection above baseline.

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68
Q

What part of the ventricles is first to repolarize?

A

The epicardium of the apex.

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69
Q

Why is the T wave positive in deflection?

A

Because repolarized areas have a positive charge, therefore, a (+) net vector occurs.

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70
Q

In a vectorcardiogram, when is the vector the largest?

A

When half of the ventricle is depolarized.

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71
Q

An axis shift will also cause what to change in an EKG?

A

It will slightly prolong the QRS

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72
Q

What EKG observations are made in V1 & V6 in a RBBB?

A

V1 has a positive secondary R wave & V6 has a slurred terminal S wave.

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73
Q

What EKG observation are made in V1 & V6 in a LBBB?

A

V1 has a wide negative S wave & V6 has rabbit ears

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74
Q

What is a high voltage EKG & what causes it?

A

If the sum of Leads I-III is >4mV & usually caused by increased ventricular muscle mass either due HTN or marathon runners.

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75
Q

What will cause decreased voltages in a standard EKG?

A

Cardiac muscle abnormalities, pleural effusions, emphysema, fluid in perdicardium, & anterior-posterior rotation of the apex.

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76
Q

What are 3 causes of current of injury?

A

Ischemia, mechanical trauma, & infection.

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77
Q

Does injured tissue emit current? If so, what kind?

A

Yes, it emits negative charges throughout each beat.

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78
Q

What type of deflection for the P wave, QRS, & T wave will we see in aVR?

A

Negative P, QRS, & T wave.

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79
Q

What degree relates to aVL?

A

-30 degrees.

80
Q

What current of injury will be observed in Leads I, II, & III with a left lateral superior infarct on a standard EKG?

A

A negative deflection in Lead I, & positive deflections in Lead II & III.

81
Q

If Lead I has a + current of injury & Lead III has a – current of injury, where would the infarct be & what direction is mean vector pointing at?

A

Infarct would be in the lower lateral area of the RV & the vector would point more towards the left shoulder.

82
Q

If V2 has a prolonged depolarization & a negative deflection from the Isoelectric point, what would this be indicative of?

A

An anterior wall infarct.

83
Q

Lead II & Lead III have negative currents of injury & V2 has a + current of injury, would be what kind of infarct?

A

Posterior wall infarct

84
Q

In an uninfarcted heart, what QRS currents will be seen in V1 & V2?

A

The QRS will be negative in nature.

85
Q

What can result in recurring ischemia of a particular area recovering from a thrombus?

A

Exercise

86
Q

RV hypertrophy would result in the QRS being ____ & the T-wave being ____?

A

Widened & inverted

87
Q

Repolarization of the endocardium followed by the epicardium will be seen as, what?

A

An inverted T-wave

88
Q

What are causes covered in class of tachycardia?

A

Increased body temp, SNS stimulation (such as reflex or blood los), toxic conditions, such as ischemia or nicotine, or caffeine (not a toxin).

89
Q

How does phenylephrine affect the HR?

A

There is an SVR increase, the baroreceptors sense that & a reflex inhibition signal is send to nodal tissue to reduce HR.`

90
Q

Bradycardia is caused by ____ K+ permeability at the _____ which _____ phase 4.

A

Increased, SA node, & prolongs

91
Q

Inhibiting adenylate cyclase leads to reduced_____, which leads to HCN channels_____, which leads to a ______ phase 4.

A

cAMP, closing, & longer.

92
Q

Which rhythm leads to seeing stars, decreased filling time, & a possible drop in BP?

A

Paroxysmal SVT

93
Q

What are the treatment options for P-SVT?

A

Vagal maneuver, BB to shut some HCN channels –> slowing depolarization, CCB slowing action potential transmission, Digoxin, & a halter monitor.

94
Q

What is the cause of P-SVT?

A

Abnormal atrial excitation

95
Q

What will be observe in a Sinoatrial block?

A

Possibly no P-wave. Inverted P-wave if AP is coming from AV node, & a HR of 40-60bpm

96
Q

What are the possible causes (5) of an Atrioventricular block?

A

Ischemia of the AV nodal tissue or fibers, compression of AV bundle from scar or calcified tissue, inflammation, excessive vagal stimulation, excess digitalis.

97
Q

What do the left and right vagus nerve innervate?

A

Left supplies the AV node & right supplies the SA node

98
Q

Why are ACE inhibitors possibly prescribed after an MI?

A

ACEi are growth factor inhibitors and can slow down scar tissue formation.

99
Q

What is seen in an incomplete 2nd degree heart block, Mobitz Type I?

A

Increasing PR interval of 0.25 – 0.45sec, dropped QRS complexes.

100
Q

What is seen in Mobitz type II?

A

Fixed & long PR interval, fixed ratio for dropped beats, which can vary.

101
Q

What feedback is seen in 3rd degree HB?

A

An increase in SA node firing.

102
Q

What happens & is observed in Atrial flutter?

A

Circular coordinated action potentials, which do not come from the SA node. An atrial HR of 200+ with ventricular tachycardia.

103
Q

Compare how the Atria contribute to cardiac output in a healthy vs sick heart.

A

In a healthy heart it contributes to about 5% of CO at rest & in a sick heart it contributes to about 25% of CO.

104
Q

What are some causes of A-Flutter?

A

Ischemia, atrial hypertrophy

105
Q

How does atrial hypertrophy cause A-Flutter?

A

Parts of the atria may already have reset and when a close signal passes by it may depolarize.

106
Q

What can cause A-Fib & how is it usually treated?

A

Atrial hypertrophy, stenotic valve or regurgitation. Treated with anti-coags.

107
Q

What is the 5 & dime reflex?

A

During eye procedures if the 5th cranial nerve (Trigeminal) is pressed on it causes cranial nerve 10 (Vagus) to fire, possibly causing complete HB for a brief time.

108
Q

What happens in Stokes-Adams syndrome?

A

An irregular AV block, the 1st beat of the ventricular escape rhythm is delayed for up to 30sec due to the purkinjie fiber’s Vrm being -90 and phase 4 slope being very gradual as there are very few Na+ leak channels. During this time it is likely to faint d/t low BP. After the first beat the rhythm is relatively regular at 15-40bpm.

109
Q

What are the causes of premature atrial contractions?

A

Ischemia, irritation or calcified plaques.

110
Q

What is a radial pulse deficit?

A

Early depolarization results in less filling time & lower SV, which can be felt at the left radial artery.

111
Q

When would inverted P-waves be observed?

A

When the AP is coming from or near the AV node in PAC’s or PVC’s.

112
Q

In an action potential that originates in the middle of the AV junction, what will be seen on the EKG?

A

A missing P-wave as it’s obscured by the QRS.

113
Q

What is the source if an early & inverted P-wave are seen?

A

High AV junction source

114
Q

What is the source if a late & inverted P-wave are seen?

A

Low AV junction source

115
Q

Why are PVC’s wider & have a higher amplitude?

A

Ventricular muscle conducts slower than the purkinjie system & 1 ventricle depolarizes before the other & the currents do not cancel each other out.

116
Q

What are the causes of PVC’s?

A

Caffeine, nicotine, stress, & lack of sleep.

117
Q

Describe the EKG of a PVC?

A

Normal P wave, QRS widened & higher amplitude, & T wave inverted.

118
Q

When do the coronary arteries perfuse?

A

Diastole= End of the T wave to the start of QRS

119
Q

What is a regular QT interval & when is it considered long?

A

Regular is <40% of RR interval & >50% is considered long QT.

120
Q

An EKG says long QT interval, in basic terms what is happening?

A

Early afterdepolarization

121
Q

Relate Fast Na+ & L-type Ca2+ channels to EAD’s?

A

Dysfunctional Na+ & Ca2+ channels have not reset properly & open on their own causing an EAD.

122
Q

Relate beta agonists to EAD’s?

A

A beta agonist causes phosphorylation of Ca2+ channels, which increase sensitivity, which can cause EAD’s.

123
Q

How can antihistamines cause EAD’s?

A

1st Gen block muscarinic receptors –> decrease K+ permeability of nodal tissue –> longer time in phase 3.

124
Q

Relate hyperkalemia to DAD’s?

A

The Vrm shifts up closer to threshold & leads to increased K+ permeability thru simple Ion channels, delayed K+ & K+ir channels.

125
Q

How does low ECF K+ relate to EAD’s?

A

Closure of K+ir & delayed rectifier K+ channels lead to longer time in phase 3.

126
Q

What kind of current and voltage is used in defibrillation?

A

DC current & high voltage (increase voltage with successive shocks).

127
Q

Delineate the pathway of extreme hyperkalemia & what it leads to in relation to cardiac action potentials?

A

The Vrm shifts up & V-G K+ Ion channels do not reset. Eventually lose the ability of fast Na+ channels causing a gradual phase 0 slope. If the Vrm shifts higher, then the Ca2+ channels cannot reset either, that will lead to loss of action potential generation.

128
Q

Describe Type 1 antiarrhythmic drugs?

A

They are fast Na+ channel blockers. Manipulate speed of conduction but not the HR. – Caine drugs

129
Q

Describe type 2 antiarrhythmic drugs?

A

Beta blockers. Slow down nodal tissue via reducing HCN mediated Na+ influx during phase 4. Also, reduce the SERCA pump  longer AP, & limit phosphorylation of Ca2+.

130
Q

Describe type 3 antiarrhythmic drugs?

A

K+ channel blockers. TEA, 4,5 diamino pyridine, Amiodarone

131
Q

Describe type 4 antiarrhythmic drugs?

A

CCB’s reduce force & slow down nodal action potential.

132
Q

What does adenosine do?

A

Bind to A1 receptors & slows down HR or reset thru greatly increasing K+ conductance.

133
Q

What is inotropy & chronotropy?

A

Inotropy= increase contractile force or Ca2+ sensitivity. Chronotropy= mediates HR

134
Q

What is Dromotropy?

A

Conductance speed. Beta agonsits increase conductance speed.

135
Q

What is Lusitropy?

A

Resetting of the heart. Beta agonists speed up SERCA pumps= faster reset.

136
Q

How does general anesthesia affect arrhythmias?

A

Causes an increased sensitivity to catecholamines & a reduction of NE reuptake.

137
Q

How do CVL’s or contact with the heart affect the EKG?

A

There may be a missed beat or two.

138
Q

How does the ventilator rate relate to arrhythmias?

A

An increase in ventilator rate will cause breathing off CO2, which causes the plasma proteins to lose attached protons causing Ca2+ attraction & binding to the protein. This bond causes a decreased ionized(free) Ca2+ level. Hypoventilation may increase plasma Ca2+ but will lead to acidosis.

139
Q

How does insulin relate to arrhythmias?

A

Insulin receptors are tethered to the Na+/K+ ATPase. An increase in insulin will increase Na+/K+ ATPase cycling.

140
Q

What are the two atrial stretch reflexes called?

A

Direct atrial stretch & Bainbridge reflex

141
Q

Differentiate between Bainbridge & Direct atrial reflex?

A

Direct stretch does not rely on outside signals & can increase the HR by 15%. Bainbridge reflex is mediated via the CNS sensors that feedback via the vagus nerve to slow firing. It can increase the HR by 50%.

142
Q

What energy products are carried to the tissues by the CV system?

A

Glucose, fatty acids, cholesterol, O2

143
Q

What waste products are carried away from the tissues via the CV system?

A

CO2, urates, nitrates, acids, lactate, lactic acid.

144
Q

How is velocity measured?

A

In distance/time

145
Q

What would cardiac output be during a workout?

A

20 – 25L/min (CO increases 4-5 times during workouts)

146
Q

How is blood flow measured?

A

In volume/time

147
Q

Which system is the least linked to metabolism?

A

The renal system

148
Q

What are the #1 & #2 vascular tone regulators?

A

1 arterioles & #2 is the nervous system

149
Q

The nervous system is in contact with everything except?

A

Brain vessels & capillaries

150
Q

The arterioles determine ____ within a given _____?

A

Blood flow & system/organ

151
Q

The highest blood velocity is in the _____ & the lowest velocity is in the ______?

A

Aorta & capillaries

152
Q

Arterioles have _____ inside diameters & ____ walls?

A

Small & thick

153
Q

Larger arteries have _____ walls?

A

Thick

154
Q

Capillaries have ____ walls with ____ inside diameters?

A

Thin & large

155
Q

Veins have ____walls with a small layer of _____?

A

Thin & smooth muscle

156
Q

How long does it take blood to flow thru a capillary?

A

2-3 seconds

157
Q

Where is the highest pressure fluctuation & what is the range?

A

In the LV. 120mmHg at systole & 2mmHg @ diastole.

158
Q

When does the aortic valve close?

A

@ 100mmHg

159
Q

What is the best MAP & how is it calculated?

A

93.3mmHg. MAP= diastolic + 1/3(systolic – diastolic)

160
Q

Where is pulse pressure the second highest?

A

In the large arteries

161
Q

What is the most important reason that BP drops?

A

Blood encounters more resistance & energy is reduced.

162
Q

How is pressure lost through the pulmonary system?

A

Equal pressure is lost throughout the system.

163
Q

Why is pulmonary pressure so low?

A

There are many parallel pathways for blood to flow through. Also there is minimal resistance.

164
Q

How is resistance calculated?

A

Delta P divided by Blood Flow

165
Q

What are these two items called?

A

Left= Ultrasonic Doppler flowmeter & Right= Electromagnetic flowmeter probe

166
Q

What is the LV diastolic pressure?

A

2mmHg

167
Q

What is the normal range for SVR in CGS units?

A

800 – 1600 dynes x sec/cm-5

168
Q

How is SVR calculated in PRU?

A

(Beginning pressure – end pressure) divided by 5L/min x (80)

169
Q

What is normal wedge pressure?

A

8mmHg

170
Q

What is a normal PVRI range in CGS units?

A

40 – 180 dynes x sec/cm-5

171
Q

How are PRU converted to CGS units?

A

Take PRU units and multiple by 1333

172
Q

What is the formula for Poiseulle’s law?

A

n= viscosity, l= length of vessel

173
Q

What is a normal Hct & how do changes affect blood flow?

A

Normal is 0.4L/L & a lower Hct will decrease viscosity

174
Q

What is the formula blood flow?

A

v= velocity, d= diameter, p= density, n= viscosity

175
Q

Where is turbulent flow most likely & what decreases the chance of turbulent flow?

A

In the aorta & higher viscosity= less turbulence

176
Q

Spell the law that relates to blood flow?

A

Poiseulle

177
Q

How many capillaries do we have & what does relate to in surface area?

A

10 billion & 500 – 700 square meters of surface area

178
Q

What 2 things does vascular smooth muscle rely on?

A

ECF calcium & tone from SNS

179
Q

Which part of the CV system lacks the endothelial layer?

A

None, it is a continuous layer

180
Q

What determines constriction of upstream arterioles?

A

Tissue factors

181
Q

What all is part of the interstitial fluid?

A

Collagen, proteoglycan filaments, hyaluronic acid, & free fluid rivulets

182
Q

What is the purpose of ECF proteoglycan filaments?

A

Provide hydration & swelling pressure to tissue enabling it wo withstand compression forces.

183
Q

Arrange the following substances from lowest to highest molecular weight, Myoglobin, Albumin, Hemoglobin, Inulin, Sucrose?

A

Sucrose < Inulin < Myoglobin < Hemoglobin < Albumin

184
Q

Which is the least permeable substance, Glucose, urea, NaCl, inulin, sucrose?

A

Inulin is the least permeable substance

185
Q

What is the Delta P in capillaries?

A

20mmHg

186
Q

What is hydrostatic pressure (Pcap) & what value goes with it?

A

Physical fluid pressure inside the capillaries generated by the heart & after SVR is applied. The value is 30mmHg

187
Q

What pressure relates to interstitial fluid pressure & what are the abbreviations for it?

A

-3mmHg & Pif or Pisf

188
Q

What is the value for oncotic pressure & the abbreviations?

A

28mmHg, & πp or πcap

189
Q

What value does the interstitial fluid colloid osmotic pressure have & what are the abbreviations?

A

8mmHg & πif or πisf

190
Q

What is the average pressure along an entire capillary?

A

17.3mmHg

191
Q

What compounds constitute the oncotic pressure?

A

Albumin, globulins, & fibrinogen

192
Q

What is the Donnan effect & its contribution?

A

Charged plasma proteins that have electrolytes bind to them & keep them from crossing into the interstitial space. It contributes 9mmHg of the total 28mmHg.

193
Q

A healthy lymphatic system has an average flow rate of ____ mL/hr & can increase up to ___ times?

A

120mL/hr & 20 fold

194
Q

What is the purpose of the lymphatic system & where does it empty into?

A

Collect excessive filtration (incl. proteins, colloids, etc) & empties into the subclavian veins.

195
Q

What two conditions adversely affect Pcap?

A

HTN= increased extremity fluid &
CHF= volume expanded & getting blood out of venous system.

196
Q

What 2 conditions affect πcap?

A

Liver failure= reduced oncotic pressure &
Burns= colloids spilling into interstitial space.