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NBS1 > Test 1 Physiology- Schushke > Flashcards

Test 1 Physiology- Schushke Flashcards

1
Q

When do non-pacemaker cells depolarize?

A

only when electrical impulses initiated by the SA and AV node are transmitted to them

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2
Q

What determines heart rate?

A

SA nodal cells that spontaneously depolarize

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3
Q

Describe Phase 4 of the Nodal Cell Action Potential?

A

begins at a max of -65 and moves towards 0 until threshold is reached. As maximum diastolic potential is reached there is an initial influx of Na through the funny cation channels and there is a decrease in permeability to K+. Late in phase 4, the T type calcium channels open

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4
Q

Describe Phase 0 of the nodal cell action potential?

A

membrane potential reaches threshold, L type calcium channels open to allow calcium to enter the cell and generate an AP

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5
Q

Describe Phase 3 of the nodal cell action potential?

A

re-polarization occurs when membrane permeability to K+ increases. This cause K+ to leave the cell and the membrane potential moves toward equilibrium for K+

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6
Q

What establishes RMP of a cardiac muscle cell?

A

cardiac myocyte RMP is established by a difference in ion concentration established mainly by the Na/K ATPase exchange. Also the permeability of the cell allows K to cross more easily compared to Na, giving the inside of the cell a more negative RMP.

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7
Q

What are the permeability levels during Phase 4?

A

High K, Low Na, Low Ca

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8
Q

What are the permeability levels during Phase 0?

A

increase Na

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9
Q

What are the permeability levels during Phase 1?

A

Decreasing Na, Increasing K

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10
Q

What are the permeability levels during early Phase 2?

A

K spike, decreasing K, Increasing Ca

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11
Q

What are the permeability levels during late Phase 2?

A

Low K, Decreasing Ca

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12
Q

What are the permeability levels during Phase 3?

A

Increasing K

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13
Q

What happens when the Fast Sodium influx channels are activated?

A

At a voltage threshold of -70 Sodium diffuses along its concentration gradient and is responsible for phase O.

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14
Q

What drug blocks the Fast Sodium Channels?

A

tetrodotoxin

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15
Q

What happens during Phase 1?

A

the transient potassium efflux channel is activated due to the inside of the cell becoming more positive. This returns the membrane potential from +20 to 0. This conducts Potassium out of the cell.

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16
Q

What is responsible for Phase 3?

A

Potassium channel (Ik)

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17
Q

What is primarily responsible for Phase 2?

A

Calcium influx channel that allows ions to diffuse along their electrochemical gradient

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18
Q

What drug blocks Calcium channels?

A

Verapamil

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19
Q

What is pacemaker potential?

A

the difference between the maximum diastolic potential and threshold potential

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20
Q

Why does depolarization (phase 0) occur more slowly in pacemaker cells?

A

there are no fast sodium channels involved

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21
Q

What causes both pacemaker and non-pacemaker cells to have a rapid re-polarization?

A

high permeability to potassium

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22
Q

What slows the rate of firing of pacemaker cells?

A

drugs that block T type Ca channels

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23
Q

What decreases the conduction rate of pacemaker cells?

A

drugs that block L type Ca channels

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24
Q

Mechanical contraction of cardiac myocytes is dependent on what?

A

membrane permeability of Ca

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25
Q

Decreased Ca permeability (Ca Channel Blockers) has what effect on cardiac myocytes?

A
  1. shortens phase 2 of AP, allowing less time for actin myosin cross bridge cycling and sarcomere shortening.
  2. reduces intracellular free Ca, which causes less binding of Ca to troponin C and causes fewer myosin binding sites to be uncovered.
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26
Q

Explain sympathetic stimulation to the heart?

A

norepi binds to B1 adrenergic receptor. This stimulates adenylate cyclase to produce cAMP through G-alpha-s. cAMP binds to protein kinase A to activate the enzyme. Protein Kinase A promotes the phosphorylation of Ca channels and funny cation channels in nodal cells.

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27
Q

Explain parasympathetic stimulation to the heart?

A

release of Ach inhibits adenylate cyclase and the production of cAMP. Ach also opens ACh depending K+ channels causing hyper polarization of the heart cells and slows heart rate and reduces activity

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28
Q

How do catecholamines affect the slope of Phase 4?

A

they increase the slope by increasing the permeability of the funny channels and increasing the influx of calcium through the cell membrane.

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29
Q

How does ACh affect the slope of Phase 4?

A

decreases the funny channel and calcium channel conductances , thus decreasing the slop

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30
Q

What causes the maximum diastolic potential to become more negative?

A

Ach increases the Potassium Channel conductance which hyper polarizes the cell membrane requiring more time to depolarize to threshold.

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31
Q

What effect does Ach have on threshold potential?

A

Ach decerases permeability of Ca and raises the threshold potential

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32
Q

What effect does norepi have on threshold potential?

A

norepi increases Ca permeability and lowers the threshold potential.

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33
Q

What is the inter-atrial pathway?

A

a pathway comprise of neural like cells which conduct impulses from the SA node of the right atrium to the left atrium. This allows left and right atrium to contract synchronously

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34
Q

What is the inter-nodal pathway?

A

conducts impulses from the SA node to the AV node

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35
Q

Why is conduction through the AV node slower than in any other region of the heart?

A

It allows for complete atrial contraction and ejection of blood into the ventricles before the ventricle contracts

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36
Q

What is the AN zone of the AV node?

A

the transition zone that contains atrial muscle cells and nodal type cells.

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37
Q

What is the N zone of the AV node?

A

contains only node cells that are characterized by slow phase 4, slow rate of phase 0 depolarization and low amplitude action potential.

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38
Q

What is the NH zone of the AV node?

A

contains nodal cells and fibers of the common Bundle of His.

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39
Q

Where is the RBB located?

A

right side of IV septum

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40
Q

The anterior division of LBB conducts impulses to where?

A

left side of the septum and through the Purkinje fibers to the apex of the heart.

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41
Q

What is the purpose of the posterior division of the LBB?

A

innervates papillary muscles and causes the muscle to depolarize in the early stage of ventricular excitation.

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42
Q

What is the function of the Purkinje fibers?

A

direct the flow of impulses through the right and left ventricles and to depolarize the ventricles quickly so that the mechanical contraction is coordinated and rapid.

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43
Q

What is the directionality of depolarization in the free walls of the ventricles?

A

endocardium to epicardium

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44
Q

What is the directionality of ventricular depolarization?

A

proceeds from the apex towards the base propelling blood toward the aorta and pulmonary artery

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45
Q

What happens as the vector rotates from perpendicular toward the positive electrode?

A

the magnitude of the positive deflection increases

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46
Q

What does P wave represent in an ECG?

A

atrial depolarization

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47
Q

What does the QRS complex represent in an ECG?

A

ventricular muscle depolarization

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48
Q

What does Tp wave represent in an ECG?

A

atrial muscle re-polarization

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49
Q

What does T represent in an ECG?

A

ventricular muscle re-polarization

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50
Q

What does a U wave (when seen) represent in an ECG?

A

late ventricular muscle re-polarization

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51
Q

What is the PR segment?

A

the time between atrial muscle depolarization and ventricular muscle depolarization. This is normally the true isoelectric line

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52
Q

What is the ST segment?

A

time between ventricular muscle depolarization and ventricular muscle re-polarization

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53
Q

What does aVR record?

A

potential at the right arm compared to the combined value of left arm and left leg

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54
Q

What does aVL record?

A

potential at the left arm compared to the combined value of the left leg and right arm

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55
Q

What does aVF record?

A

potential at the left leg compared to the combined value of left and right arms

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56
Q

Describe ECG voltage?

A

ECG voltage is inversely proportional to the square of the distance from the heart to the electrode

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57
Q

What is the most common MEA of ventricular depolarization?

A

toward the apex of the heart in the direction of lead II at 60 degrees

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58
Q

Where is the MEA usually located on a hex axial system?

A

-30 to +120

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59
Q

If the MEA is located between -30 to -90 what has happened?

A

There has been a left shift deviation

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60
Q

If the MEA is located between +120-+180 what has happened?

A

there has been a right shift deviation

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61
Q

What are the common causes of a left shift deviation?

A

LV hypertrophy, LBB block, High diaphragm (obesity, pregnancy), or right side infarct

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62
Q

What are the common causes of a right shift deviation?

A

RV hypertrophy, RBB Block, flat diaphragm (thin build, emphysema), and left side infarct.

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63
Q

What is the value for bradycardia?

A

Less than 60 ppm

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64
Q

What is the value of a tachycardia?

A

greater than 100 bpm

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65
Q

What determines atrial “F” waves?

A

HR greater than 250, but less than 350

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66
Q

What determines atrial “f” waves?

A

HR greater than 350

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67
Q

Where does a sinus rhythm originate?

A

SA node

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68
Q

Where does an atrial rhythm originate?

A

atrial muscle

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69
Q

Where does the supra ventricular rhythm originate?

A

above the ventricles

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70
Q

where does the ventricular rhythm originate?

A

from the ventricle

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71
Q

Where does the nodal rhythm originate?

A

junctional zone

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72
Q

Where does the paroxysmal rhythm originate?

A

suddenly start and stops

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73
Q

What could be the reason for a conduction block beyond .2 sec?

A

conduction block

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74
Q

what is physiological sinus arrhythmia?

A

physiological reflex associated with inspiration.

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75
Q

Describe physiological sinus arrhythmia?

A

as we inspire, pulmonary stretch receptors are stimulated to transmit inhibitory vagal signals to the respiratory center to stop inspiration. This also inhibits vagal neural tone to the SA node allowing heart rate increase

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76
Q

What is an AV heart block?

A

delay or interruption in conduction between atria and ventricle

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77
Q

Describe first degree AV block?

A

all components of ECG are within normal limits, except the PR interval which is prolonged (greater than .2)

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78
Q

What is the mechanism behind 1st degree AV block?

A

delay in electrical impulses at the level of the AV node

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79
Q

What is a second degree AV block?

A

when some, but not all, atrial impulses are blocked from reaching the ventricles.

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80
Q

What does the ECG of a second degree AV block look like?

A

Not all P waves are followed by a QRS complex. The PR interval will lengthen with each cycle until a P wave appears without a following QRS complex

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81
Q

What is Second Degree AV Block Type I?

A

Second degree AV block that almost always occurs at the AV node

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82
Q

What causes a second degree AV block Type I?

A

increased parasympathetic tone or cardio-suppressant drug

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83
Q

What is second degree AV block Type II?

A

occurs below the level of the AV node (usually at the bundle branch)

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84
Q

What normally causes second degree AV block Type II?

A

organic lesion in the conduction pathway.

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85
Q

What does the ECG of a second degree AV block Type II normally look like?

A

atrial rate is greater than ventricular rate, ventricular rhythm is irregular, more P waves than QRS complexes,

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86
Q

What is a third degree AV block?

A

a complete AV block where there is no conduction of impulses between the atria and ventricles that can occur at the AV node, Bundle of His, or Bundle Branches

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87
Q

What does the ECG of a third degree AV block look like?

A

No PR interval, QRS may be narrow or wide depending on site of escape pacemaker.

88
Q

What is a Bundle Branch Block?

A

a delay or block in one of the bundle branches where the ventricles will be depolarized asynchronously.

89
Q

What is the conduction pathway in a bundle branch block?

A

impulse travels down the unblocked bundle branch and stimulates that ventricle, the impulse then travels from cell to cell through the myocardium to stimulate the other ventricle.

90
Q

What does the ECG of a bundle branch block look like?

A

QRS is wider than normal and the ventricle with the blocked bundle branch is the last to be depolarized

91
Q

What Wolff-Parkinson-White Syndrome?

A

The PR interval is shorted due to electrical impulse from the atrial tissue traveling quickly across the AV ring through an accessory pathway.

92
Q

What is the ECG pattern in WPW syndrome?

A

delta wave seen as in initial early upslope in the QRS complex and a PR interval of less than .12 sec.

93
Q

What is atrial fibrillation?

A

occurs due to multiple irritable sites in the atria firing at a rate of 400-600 times per minute that results in depolarization of small islets of atrial myocardium instead of a whole atria.

94
Q

What characterizes Afib?

A

no identifiable P waves, erratic wavy baseline, no measurable PR interval. QRS duration less than .1 sec

95
Q

What defines ventricular tachycardia?

A

at least 3 consecutive ventricular complexes with a rate of more than 100 beats per minute.

96
Q

What are the ECG characteristics of Ventricular tachycardia?

A

No p waves or PR interval, and QRS duration of less than .12 sec

97
Q

What is Ventricular Fibrillation?

A

chaotic ventricular rhythm in which multiple areas within the ventricles exhibit varying degrees of depolarization and re-polarization. (myocardium appears to quiver due to ventricles not contracting as a unit)

98
Q

What are the characteristics of Vfib ECG?

A

no pattern or regularity in rhythm, no discernible wave or durations

99
Q

Describe the ECGs seen in a premature ventricular contraction?

A

reduced RR interval, QRS complex not preceded by a P wave, QRS complex may be wider than normal, abnormally shaped QRS complex, T wave may be abnormal, compensatory pause

100
Q

Describe the re-entry phenomenon?

A

when adjacent areas of myocardium have different conduction velocities and refractory periods. An AP can proceed in a circuit as the refractory periods expire. This alteration in the normal conduction pathway results in continual circular depolarization. This can lead to refractory mismatch and cell depolarizing at different times leading to fibrillation.

101
Q

Why do we most often see focal ischemia in the endocardium?

A

Because vascularature runs from the outside in, so endocardium becomes ischemic first

102
Q

What are the two consequences of ischemia?

A

reducing oxygen deliver (causing the Katp channels to leak and slows the Na-K ATPase and 2. diminishes the washout of K+ leading to a less negative RMP which causes us to have a current in diastole when there shouldn’t be one

103
Q

what effect does focal ischemia have on the cardiac myocyte APs?

A

The RMP is less negative in focal ischemia, which leads to fewer of the fast Na+ channels to close. When an AP is conducted, there is less rapid depolarization and the inside of the ischemic cells do not become positive relative to the outside.

104
Q

What is the sure sign of ischemia in an ECG?

A

net negative deflection during systole during the ST segment

105
Q

Inferior portion of the heart will be seen in what leads?

A

2,3, and aVF

106
Q

A problem in leads 2,3 or aVF shows damage to what structures?

A

Right coronary, right atrium/ventricle, SA node, AV node, Bundle of His,

107
Q

The septal portion of the heart is seen in what leads?

A

V1, V2

108
Q

An abnormality in V1 or V2 shows damage to what structure?

A

LAD–> anterior and lateral portion of left ventricle, IV septum, RBB, and anterior LBB

109
Q

Anterior portion of the heart is seen in what leads?

A

V3 and V4

110
Q

Lateral portion of the heart is seen in what leads?

A

V5, V6, I and aVL

111
Q

abnormalities in leads I, aVL, V5 and V6 shows damage to what structure?

A

circumflex artery, Left atrium, lateral left ventricle, SA node, AV node

112
Q

what is contractility?

A

the ability of a cardiac muscle to generate force for any given fiber length

113
Q

What does contractility depend on?

A

cytosolic calcium

114
Q

Describe Cardiac contraction?

A
  1. initiation during plateau phase as Ca enters the L type calcium channels
  2. AP travels along membrane of T tubules and Ca enters the cell causing a small rise in Ca in the gap between the sarcolemma and the junctional SR.
  3. Increase in Ca activates Ca release channels in the SR (ryanodine receptors)
  4. Rapid increase in Ca occurs and tension starts to develop (calcium induced calcium release)
  5. Generation of tension occurs by the sliding filament mechanism of muscle contraction
115
Q

What happens to the calcium that is not released from the extracellular space to go through the L type channels?

A

binds to calsequestrin

116
Q

What determines the amount of Ca released during cardiac muscle contraction?

A

depends n how much is stored in the SR and the number of release channels activated

117
Q

Describe cardiac muscle relaxation?

A
  1. a rise in Ca above resting level activates ATP-dependent Ca pumps in the tubular part of the SR and Ca is pumped back into the SR
  2. as membrane potential re-polarizes and voltage dependent Ca channels inactivate, Ca decreases, and Ca dissociates from troponin C and the muscle relaxes.
  3. During relaxation, excess Ca is removed from the cell by the Na-Ca exchanger
118
Q

What determines how much calcium is removed through the Na-Ca exchanger in cardiac muscle relaxation?

A

electrochemical gradient of Na to remove 1 Ca for each 3 Na ions that enter the cell

119
Q

What is normal diastolic BP?

A

80

120
Q

What is normal systolic BP?

A

120

121
Q

The pressure in the atria is equivalent to what pressure?

A

the pressure in the vena cava

122
Q

What gives the best estimate for filling pressure of the left side of the hearT?

A

pulmonary wedge pressure

123
Q

Pulmonary wedge pressure should be similar to what pressure?

A

pressure in the left atria

124
Q

What is the pathway followed by a Swan Ganz catheter?

A

introduced in vena cava (via subclavian)–> right atrium–> right ventricle –> pulmonary artery–> wedged in a small lung artery

125
Q

What does a Swan Ganz catheter measure?

A

pulmonary wedge pressure

126
Q

What happens then the right heart fails to move blood?

A

CVP/right atrial pressure becomes too high

127
Q

What happens when the left heart fails to move blood?

A

PWP becomes too hight

128
Q

What is an affect of high CVP and PWP?

A

lung edema and death by suffocation

129
Q

Describe pressures when the semilunar valve is open?

A

ventricular pressure is greater than arterial pressure

130
Q

Describe pressures when semilunar valve is closed?

A

arterial pressure is greater than ventricular pressure

131
Q

When the atrioventricular valves are open what are the pressures?

A

atrial pressure is greater than ventricular pressure

132
Q

What are the pressure relationships with the atrioventricular valves are closed?

A

ventricular pressure is greater than atrial pressure

133
Q

Describe right and left heart synchrony?

A

right atria contracts, then left atria contracts. Left ventricle contractions, then right ventricle contracts. Right ventricle ejects, then left ventricle ejects. Left ventricular ejection ends, then right ventricular ejection ends.

134
Q

What is after load?

A

the load that the ventricles must work against to move blood from the ventricle into the artery.

135
Q

What is the main component of after load?

A

diastolic blood pressure

136
Q

What are the the steps in the cardiac cycle?

A
  1. systole: period of isovolumic contraction
  2. systole: period of ejection (semilunar valve open)
  3. diastole: period of isovolumic relaxation
  4. diastole: passive ventricular filling (AV valve open)
  5. diastole: active ventricular filling (AV valve open)
137
Q

What is the S1 heart sound?

A

blood flowing against the mitral valve (lub)

138
Q

What is the S2 heart sound?

A

blood flowing against the aortic valve (dub)

139
Q

What is the S4 heart sound?

A

you hear the blood vibrating against the rigid ventricle walls (pathogenic)

140
Q

What is the S3 heart sound?

A

reduced compliance of ventricular wall, but not always pathogenic, often seen in endurance athletes.

141
Q

How do you observe jugular pulsations in a healthy subject?

A

place the head below the heart to distend the right atrium, superior vena cava, and jugular veins with blood. Now changes in the right heart pressures and volumes will initiate reflected pulses in the jugular volume and affect its dissension

142
Q

When will you see a large jugular a wave pulse?

A

Cannon wave seen during complete AV heart block (third degree)

143
Q

When does the a wave of jugular pulse occur?

A

immediately after depolarization of right atrium (p wave of ECG) and due to mechanical contraction of right atrium

144
Q

What is the c wave in jugular pulse?

A

occur immediately after QRS complex and S1 heart sound. results from sudden increase in right ventricular pressure due to contraction of right ventricle

145
Q

what is the v wave in jugular pulse?

A

lower amplitude pulse caused by passive filling of jugular vein throughout ventricular systole and sudden outflow of blood from the jugular vein into right atrium when right ventricular pressure falls.

146
Q

What does the jugular venous pulse look like in an stenotic tricuspid valve?

A

large a wave (high pressure by right ventricle due to stenosis in valve)

147
Q

What are the possible causes of a stenotic tricuspid valve?

A

rheumatic fever or high afterload

148
Q

What does the jugular venous pulse of an insufficient tricuspid valve look like?

A

large c-v waves throughout right ventricular contraction due to blood being pumped back into the right atrium and jugular vein rather than into the pulmonary artery

149
Q

What causes an insufficient tricuspid valve?

A

persistent pulmonary hypertension or ventricular dilation

150
Q

What happens in an insufficient tricuspid valve?

A

with each contraction of the right ventricle, blood is ejected back into the right atrium. This increase in blood volume increase the pressure in the right atrium and jugular vein.

151
Q

When and where do we hear S1?

A

during isovolumic contraction near the apex of the heart, left 4th or 5th ICS, mid clavicular line.

152
Q

What initiates S2?

A

oscillations and vibrations of the decelerating blood during the end of reduced ejection when the semilunar valve close and incisura occurs.

153
Q

What are the sequence of events in the splitting of the 2nd heart sound?

A
  1. decrease in intrathoracic pressure (more negative)
  2. increase in transmural pressure across heart
  3. increase in right ventricular volume (more blood returning to IVC)
  4. increase in stroke volume
  5. increase in ejection time (vessels more able to absorb blood)
  6. increase in pulmonary valve closing even later
  7. split of S2 heart sound (aortic closes before pulmonic)
154
Q

Describe a fixed split S2?

A

result of delayed right ventricular contraction (RBBB) or prolonged right ventricular ejection. Inspiration will widen this split

155
Q

What is a paradoxical split of S2?

A

P2 occurs before A2. The second heart sound can be heard during expiration, but not during inspiration.

156
Q

What causes a paradoxical split of S2?

A

delated left ventricular contraction (LBBB) or prolonged left ventricular ejection

157
Q

What are systolic murmurs?

A

vibrations of the cardiohemic system which occur during systole, between S1 and S2.

158
Q

What usually occurs with systolic murmurs?

A

stenosis of semilunar valves or insufficiency of AV valves

159
Q

What is a holosystolic murmur?

A

mild to moderate AV insufficiency that results in turbulence throughout systole

160
Q

What causes mid-diastolic murmurs?

A

mitral or tricuspid stenosis

161
Q

What causes early diastolic murmurs?

A

semilunar valvular insufficiency

162
Q

What are the characteristics of a systolic murmur cause by aortic stenosis?

A

high ventricular pressure, low aortic pressure, left hypertrophy (back up into right heart), and left axis deviation

163
Q

What are the characteristics of a diastolic murmur caused by mitral stenosis?

A

high atrial pressure (PWP) and right congestive heart

164
Q

What are the characteristics of a diastolic murmur caused by aortic insufficiency?

A

low diastolic pressure, large pulse pressure, and high EDV

165
Q

What are the characteristics of a systolic murmur caused by mitral insufficiency?

A

high atrial pressure (PWP), EDV and pressure is high, and may be a prolapsed valve.

166
Q

What are the outcomes of aortic stenosis?

A

left heart failure, back pressure into lungs, pulmonary hypertension, and right heart failure.

167
Q

Mitral stenosis leads to what?

A

stiff mitral valve, reduced cardiac output, pulmonary hypertension leading to right HF, and central venous return increases leading to peripheral edema

168
Q

What are the outcomes of aortic insufficiency?

A

angina, palpitations, pulmonary hypertension, peripheral pulsations due to large pulse pressure, A fib due to refractory mismatch, left ventricular hypertrophy.

169
Q

What are the outcomes of mitral insufficiency?

A

right HF, pulmonary hypertension, left ventricular hypertrophy due to increase in pulmonary wedge pressure

170
Q

What is cardiac output?

A

HR x SV

171
Q

What is stroke volume formula?

A

EDV-ESV

172
Q

What is ESV?

A

the little bit of blood left after contraction (residual)

173
Q

What is the Cardiac Index formula?

A

CO/body surface area

174
Q

What is Ejection Fraction?

A

percentage of EDV that is ejected

175
Q

What is the ejection fraction formula?

A

EF= (EDV-ESV)/ EDV

176
Q

What is the normal range of CO in adults?

A

3.5-5 L/min

177
Q

What is a normal ejection fraction?

A

50-66%

178
Q

What is a normal value for ESV?

A

50-60 mls

179
Q

What is the normal range for EDV?

A

100-120 ml

180
Q

What is the normal value of O2 consumption in a 70kg man?

A

250ml O2/min

181
Q

What is the normal value for pulmonary artery (venous blood) O2?

A

15ml O2/dl blood

182
Q

What is the normal value for pulmonary vein (arterial blood) O2?

A

20 ml O2/dl blood

183
Q

What is the formula for flow?

A

O2 consumption (ml O2/min)/ O2 differences (venous-arterial)

184
Q

What factors affect EDV?

A

filling pressure (CVP, PWP), filling time (HR), and ventricular compliance

185
Q

What factors affect ESV?

A

heart rate, preload, after load, contractility

186
Q

What factors affect intrinsic regulation?

A

threshold potential, max diastolic potential, and slope of phase 4

187
Q

What factors affect extrinsic regulation?

A

ANS (positive and negative chronotrope) and humoral factors (ex: norepi, epi)

188
Q

What does a positive chronotrope do?

A

increase heart rate by increasing the slope of phase 4 depolarization of the SA node.

189
Q

What are examples of positive chronotropes?

A

mainly norepinephrine

190
Q

What does a negative chronotrope do?

A

increase conductance of K through acetylcholine-activated K channels which causes hyper polarization of the RMP requiring a long depolarization

191
Q

What is an example of a negative chronotrope?

A

increase in right vagal stimulation to the SA node

192
Q

What is the application of Frank Starling on Cardiovascular?

A

as the EDV of the atria or ventricles increases, the maximum pressure generated by the cardiac chamber will increase

193
Q

What is the Frank Starling mechanism dependent on?

A

initial muscle length, results in an increase in the peak pressure generated by the muscle and in an increased stroke volume, and cellular basis (increase in the number of cross bridges formed, optimum arrangement of actin and myosin, and increased sensitivity to intracellular Ca)

194
Q

What is pre-load?

A

blood volume in the heart ventricles at the end of diastole (EDV)

195
Q

What is pre-load dependent on?

A

filling pressure (CVP for right heart and PWP for left heart), filling time (inverse HR), and residual volume (ESV)

196
Q

What increases in pre-load?

A

high CVP, high PWP, and a slow HR

197
Q

What is the main component of after load?

A

aorta’s diastolic blood pressure (mainly left ventricle)

198
Q

What is after load dependent on?

A

preload, TPR, and the stiffness of the ventricle wall

199
Q

What contributes to high after load?

A

high diastolic BP, large preload, high TPR, and stiffer ventricular wall.

200
Q

What factors can increase contractility of the heart?

A

increase calcium entry from outside the cell, increase release of Ca from the SR, or reduced pumping of cytosolic calcium out of the cell or back into the SR

201
Q

What contributes to ESV?

A

preload, heart rate, contractility, and after load

202
Q

What is Inotropy?

A

a measure of contractility and indicates ventricular contraction efficiency

203
Q

What does a positive inotrope do?

A

increase contractility by increasing intracellular Ca

204
Q

What is the effect in an increase in the inotropic state of the heart?

A

greater increase in the pressure developed within the ventricle, increase in stroke volume, and an increase in EF

205
Q

What effect does a positive inotrope have on the Frank Starling curve?

A

shift upward and to the left

206
Q

What are the normal values for CO?

A

3.5-5

207
Q

What is a normal value for EF?

A

1/2-2/3

208
Q

What effect does a positive inotrope have on muscle fibers?

A

causes the muscle fibers to shorten to a greater extent, thus decreasing ESV

209
Q

What is the effect of NE?

A

increases heart rate by acting on Ca. It increases calcium entering the cell and increasing Ca released from the SR. In addition, this increase in Ca increases the calcium-calmodulin complex, which causes in increase of phosphorylation of MLCK. Lastly, phospholambin is phosphorylated causing an increase in the speed of the calcium pump. This increases the force of contraction and decreases the time duration of the contraction

210
Q

What effect do cardiac glycosides, like digitalis, have on the heart?

A

they reduce the electrochemical gradient for sodium across the cell membrane. This causes less Ca to be removed from inside the cell and the intracellular concentration of Ca stays high longer, promoting increased contractility.

211
Q

What are examples of positive inotropic agents?

A

adrenergic agonists, cardiac glycosides, high extracellular Ca, low extracellular Na, and increased heart rate

212
Q

what are examples of negative inotropic agents?

A

Ca channel blockers, low extracellular Ca, and high extracellular Na

213
Q

What is dobutamine?

A

a catecholamine with only beta effects. It’s a positive inotrope. It increases contractility without increase O2 demand of tachycardia.

214
Q

Describe the function of Nitroglycerin?

A

dilates coronary arteries improving perfusion of ischemic myocardium. It is the drug of choice for angina pectoris

215
Q

Describe the function of Sodium nitroprusside?

A

peripheral vasodilator affecting both the arterial and venous systems. Used to reduce after load

NBS1 (6 decks)

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