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Pathophysiology I - Exam 3 (Final) > Cardio Module 2 > Flashcards

Cardio Module 2 Flashcards

1
Q

Define Syncytium

A

a cardiac muscle fiber arrangement that allows rapid spread of electric energy. The arrangement is ‘interconnected’. It allows the action potential of one cell to move rapid fire to others nearby, saving energy.

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2
Q

Define Automaticity

A

The ability to spontaneously depolarize to action potential threshold

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3
Q

Define Rhythmicity

A

The regular generation of action potential by the heart

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4
Q

Define NSR

A

Normal sinus rhythm. A healthy heart that’s beat originates from the SA node at approx. 70 bpm

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5
Q

Define Bradycardia

A

slowed HR

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6
Q

Define Tachycardia

A

elevated HR >100bpm

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7
Q

The most frequent spontaneous electrical activity of the heart is limit to what specialized area

A

The SA node

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8
Q

Where is the SA node located?

A

In the right atrium

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9
Q

How does the SA node work?

A

Spontaneous electrical activity here occurs due to a constant leakage of Na+ during diastole. When the SA node reaches a certain threshold (due to the Na+ influx) depolarization occurs and spreads throughout the atria resulting in atrial contraction (systole)

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10
Q

Describe the electrical pathway of a heartbeat.

A

Starts at the SA node in the atria and goes down specific intermodal atrial pathways to the AV node. From there the AV node sends the impulse thru the fibrous skeleton, through the septum and into the ventricular walls. It goes thru the bundle of His and splits to the R/L bundle branches and eventually gets to tiny Purkinge fibers

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11
Q

About how long is the electrical conduction time for atrial and ventricle depolarization

A

About 0.2 -0.3 seconds

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12
Q

Why is the pause in the AV node important

A

It allows for the mechanical cross bridge cycling of the atrium to do its kick and contract

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13
Q

Break down the 0.2 -0.3 seconds of electrical conduction time

A
  1. 1 sec for the atria to depolarize
  2. 1 sec for a rest at the AV
  3. 1 sec for ventricle to depolarize
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14
Q

Where is depolarization of the initiated

A

At the SA node in a healthy heart

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15
Q

What are factors that increase/decrease the rate of the pacemaker of the heart?

A

Increases - Fever, various drugs, parasympathetics down, sympathetics up and inspiration
Decreases - Parasympathetics up, sympathetics down (vagus influence), meds ike digitalis

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16
Q

What is Respiratory Sinus Arrythmia

A

A normal occurance that is the result of the inspiration/vagus reflex. Inspiration briefly decreases vagus tone to the heart thus increasing HR

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17
Q

Name the 3 internodal pathways in the heart

A

Anterior, middle and posterior nodal pathways

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18
Q

Anterior internodal pathway (AKA and where does it travel)

A

AKA - Bachmann’s bundle. It transmits directly to the left atria

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19
Q

What does the posterior intermodal do

A

Conducts energy from the SA node to the AV node

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20
Q

What does that 0.1 sec delay at the AV node do. What is it influenced by

A

It slows the conduction rate of the node and allows for the mechanical contraction of the atria (atrial kick). The sympathetic NS can speed up the delay. The parasympathetic NS will lengthen the delay

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21
Q

WHere is the AV node located?

A

In the right posterior portion of the interventricular septum (just superior to the tricuspid valve and anterior to ostium of the coronary sinus

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22
Q

What is the bundle of His?

A

The continuation of the AV node. It’s located in the posterior border of the interventricular septum and serves as the origin of the R/L bundle branches

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23
Q

Where do the bundle branches run

A

Down the interventricular septum

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24
Q

What are the Purkinje fibers and what do they do

A

Terminal branches of the R/L bundle branches that decend to the ventricular apices. They RAPIDLY transmit depolarization throughout the ventricles (in about 0.1 second throughout the whole ventricle)

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25
Q

Number of ‘leads’ in an EKG recording

A

12 leads

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26
Q

What is the P wave

A

The part of the EKG wave representing the initial atrial depolarization. When the valves between the atria and ventricles open, and 70% of the blood in the atria falls through with the aid of gravity, but mainly due to suction caused by the ventricles as they expand. The Action potential travels throughout the atria via the intermodal atrial pathway.

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27
Q

PR interval

A

Represents atrial depolarization and conduction through the AV node. It’s the duration from the start of the atrial activation to the start of ventricular activation (including the brief pause in the AV node). It’s measured from the beginning of the P wave to the beginning of the Q or R wave

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28
Q

QRS complex represents_______

A

Ventricular depolarization and atrial repolarization

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29
Q

The Q in the QRS complex represents ?

A

Septal depolarization (when the action potential goes down the septum of the heart). Its a small negative wave immediately before the large QRS complex. It’s the time where the electrical stimulus passes thru the bundle of His, before it travels down the two bundle branches.

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30
Q

The R in the QRS complex represents

A

Ventricular depolarization. It’s the largest wave and happens when the electrical impulse passes thru the main portion of the ventricular walls. Since the walls are thick, it requires the most voltage.

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31
Q

The S in the QRS complex represents

A

Depolarization of the Purkinje fibers. Its the second slightly larger negative deflection after the large R wave.

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32
Q

What waves may you not see on an ECG?

A

May not always see the Q or S wave

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33
Q

What is the ST segment

A

The brief period of no electrical (Isoelectric) activity due to the ventricles reaching full depolarization. Here the line is flat. It represents the mechanical cross bridge cycling.

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34
Q

the T wave represents

A

Ventricular repolarization. It represents a smaller positive deflection

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35
Q

What is the U wave?

A

It represents repolarization of papillary muscles or Purkinje fibers. (also remnants of ventricular repolarization). May not always be seen and origin is debated.

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36
Q

What does the QT interval represent?

A

Represents ventricular depolarization and ventricular repolarization. When the ventricle contracts and relaxes

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37
Q

What is the ST interval

A

Different from the ST segment, it represents ventricular repolarization. The time that allows for the cross bridge cycling

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38
Q

How do you measure the ST interval?

A

the QT interval - the QRS duration

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39
Q

What could you see on an ECG if there is an AV node block.

A

An flatter and longer PR interval

40
Q

What is responsible for the sight negative dip in the Q wave.

A

The fact that left bundle branch depolarizes slightly before the right. The positive deflection goes slightly toward the right

41
Q

What’s the difference between segments and intervals.

A

Segments are periods between waves and an interval includes one or both waves

42
Q

When might you see an enlarged QRS duration

A

V-fib, hyperkalemia, bundle branch block

43
Q

When might you see an elevated/depressed ST segment

A

The ST segment represents the time btwn the spread of the impulse thru the ventricle and ventricular repolarizing.
ENLARGED - Potential acute MI, ischemia
DEPRESSED - Potential ischemia (myocardium received insufficient O2), acute posterior MI

44
Q

A flat or elevated T wave could represent? (why?)

A

Flat - Potential ischemia or hypokalemia. Elevated - hyperkalemia. Repolarization is influenced by potassium. Too much or little could cause arrhythmias

45
Q

A prominent U wave could mean what?

A

Hypokalemia

46
Q

What is a heart block

A

A complete or partial interruption of conduction between atria and ventricle

47
Q

What happens with a 1st degree heart block

A

All atrial impulses reach the ventricle but take a long time. The most mild of the different kinds of heart blocks

48
Q

What will a 1st degree heart block look like

A

An elongated PR interval

49
Q

What happens with a 2nd degree heart block

A

Some but not all atrial impulses reach the ventricles. Therefore it will not have ventricular depolarization for every atrial depolarization.

50
Q

What will a 2nd degree heart block look like?

A

3 P waves followed by a QRS complex (Would be a 3:1 block)

51
Q

What happens with a 3rd degree heart block

A

Complete disruption of conduction between atria and ventricles. Ventricles become pacemakers, usually at 35-34 bpm while atrial beating at a rapid rate

52
Q

What will a 3rd degree heart block look like

A

Will see many P waves and an occasion QRS wave showing up.

53
Q

Ventricular tachycardia is defined as

A

Three PVCs or more in a row on an ECG.

54
Q

What is an example of a Ectopic foci

A

PVC (preventricular contraction)

55
Q

What is an Ectopic foci

A

When the myocardium in the ventricle spontaneously depolarizes. The result is an unexpected QRS between normal sinus rhythm on an ECG.

56
Q

What is Atrial tachycardia?

A

A form of supraventricular tachycardia (SVT). Rapid heart rate originating in the atria. Less deadly than ventricular tachycardia. The heart goes so fast it loses the ability to pump blood and there is a stasis in blood which increases a risk for clots

57
Q

Definition of atrial flutter

A

200-350 action potentials per minute

58
Q

Definition of atrial fibrillation (A-fib)

A

> 300-350 action potentials per minute. Has a really chaotic and uncoordinated depolarization. It’s the most common arrhythmia encountered in clinical practice

59
Q

Despite the number of action potentials with Atrial flutter and A fib, the maximum bpm is…

A
  1. The AV node and ventricles can’t keep up and ‘max out’ at 200.
60
Q

What is ventricular tachycardia?

A

Rapid HR originating in the ventricles. Defined as 100 bpm and > 3 irregular beats (PVCs) in a row

61
Q

What is ventricular fibrillation

A

Rapid, chaotic uncoordinated ventricular contractions. Functionally heart cant’ act as a pump and it can be fatal in minutes. A major cause of MIs

62
Q

What are the 2 types of Cardiac Action Potentials?

A

Slow response AP’s - occur in the nodal tissue (SA and AV nodes). It can automatically depolarize without anything telling it to. Unstable resting membrane potential
Fast respons AP’s - occur in the Purkinje fibers and myocardial cells of atria and ventricles. Stable resting membrane potential. Almost instantaneous

63
Q

What are the intrinsic and extrinsic factors that influence the Cardiac cell AP’s

A

1) Autonomic nervous system (parasympathetic, sympathetic)
2) Pharmaceuticals -Anti-arrhythmic meds.
3) ECF ion concentration (Sodium, Potassium, and Calcium)

64
Q

What are the 3 phases of the Slow response of Action Potential

A

1) Phase 4 (slow depolarization)
2) Phase 0 (upstroke)
3) Phase 3 (repolarization)

65
Q

Describe Phase 4 of the Slow response Action potential

A

The slow increasing of cell membrane potential. Called the leaky membrane or funny circuit. Its driven by the rate of sodium influx that depolarizes the membrane and slows its Na+ channels. Once membrane potential reaches a threshold it triggers an action potential

66
Q

Describe the Phase 0 of the slow response Action potential

A

When a threshold is reaches the calcium channels open that cause a rapid fire of depolarization of the membrane during the action potential. Represents the positive deflection. The amount of K+ that is expelled influences how much of a dip in the wave.

67
Q

Describe the Phase 3 of the slow response Action potential

A

This is the repolarization phase represented by an influx of Potassium travelling out of the cell. This repolarization brings the membrane down back to its resting potential

68
Q

What are the 5 phases of the Fast Response Action Potential

A 
Phase 4 - resting membrane potential
Phase 0 - Upstroke
Phase 1 - Initial repolarization
Phase 2 - Plateau
Phase 3 - Repolarization
69
Q

Describe the Phase 4 of the Fast Response action potential

A

Inward and outward currents of K+ are maintained in an equilibrium. Calcium and sodium channels are closed

70
Q

Describe the Phase 0 of the fast response action potential

A

Action potential from adjacent cardiac cell depolarizes the membrane to threshold voltage (approx. -70mV). Membrane potential ‘blasts off’. Rapid inward flow of Na+ into the cell via fast NA+ channels that depolarize the membrane

71
Q

Describe the Phase 1 of the fast response action potential

A

Initial outflow of K+ out of cell via transient K+ channels begins to repolarize the membrane

72
Q

Describe the Phase 2 of the fast response action potential

A

Ca+2 flows into cell via ‘slow long lasting calcium channels’ that cause a plateau in the repolarization. This essential prolongs mechanical contraction which allows for adequate ejection for ventricles

73
Q

Describe the Phase 3 of the fast response action potential

A

K+ out of the cell combined with inactivation of ‘slow long lasting calcium channels’ repolarize the membrane back down to resting membrane potential

74
Q

What is the driving force for the Slow vs. the Fast response action potential

A

Slow - Calcium

Fast - Sodium

75
Q

In the Fast response action potential, how does the different phases match up with an EKG wave

A

Phase 4 - P wave
Phase 0 & 1 - QRS complex (initial depolarization)
Phase 2 - ST segment (corresponds to plateau)
Phase 3 to 4- T wave (repolarization)

76
Q

What parts are the heart are innervated by the parasympathetic system?

A

It innervates the SA/AV and atria ONLY. (sparse innervation in the ventricles)

77
Q

What parts of the heart are innervated by the sympathetic nervous system?

A

It innervates the atria and ventricles (including the nodes)

78
Q

What is the parasympathetic action on the heart

A

Greatly influences (lowers) the HR (chronotropy) and conduction velocity (dromotropy) .Small effect (lowers) the contractibility (Inotropy) and relaxation (Lusitropy)

79
Q

How does parasymathetics respond to the atria?

A

!) Promote/prolong K+ efflux out and inhibit Na+ and Ca+2 influx into pacemaker cells
2) Primary effect - hyperpolarizes cell membranes (due to K+ efflux) and increases the duration of Phase 4 (due to inhibited Na+ and Ca+2 influx into pacemaker cells) (that all slows the heart rate down)

80
Q

How does parasympathetics respond to the ventricles

A

They don’t

81
Q

What is the sympathetic action on the heart

A

Greatly influences (raises) the HR (chronotropy), the contractibility (Inotropy) and relaxation (Lusitropy). Small effect (raises) the conduction velocity (dromotropy) .

82
Q

How does the sympathetic system respond to the heart

A

Prolonged Ca+2 influx into pacemaker and cardiac muscle cells in both the atria and ventricles will decrease the duration of Phase 4, (which speeds up the HR)

83
Q

What are the 4 main classes in the Vaughan Williams classification of antiarrhythmic agents

A

1) Class I agents (Sodium channel blockers)
(IA - moderate) (IB - weak) (IC - Strong)
2 Class II agents (Beta blockers)
3) Class III agents (Potassium channel blockers)
4) Class IV agents (Calcium channel blockers)

84
Q

What is the mechanism of Class I agents

A

Sodium channel blockade - Reduce phase 0 slope and peak of action potential

85
Q

What is the mechanism of Class II agents

A

Block sympathetic activity on nodal cells and myocardial cells. Reduce rate and conduction.

86
Q

What is the mechanism of Class III agents

A

Delays/prolongs repolarization (phase 3) and thereby increase action potential duration and effective refractory period. Prolongs K+ efflux

87
Q

What is the mechanism of Class IV agents

A

Blocks L-type (long lasting) calcium channels; most effective at SA and AV nodes. Slows rate of depolarization of nodal cells (Phase 0) and inhibits plateau (Phase 2) of cardiac muscle cells. Lowers HR and contractility

88
Q

What is potassium’s major effect on the heart?

A

It alters repolarization.

89
Q

Hyperkalemia can result in…

A

Bradycardia

90
Q

Hyperkalemia (elevated K+) can result in…

A

Bradycardia (severe can be rapidly fatal)

91
Q

How would excess K+ (hyperkalemia) influence the action potential and slope of EKG

A

HR slows due to slower conduction velocity. So you’d see a prolonged P wave, PR interval and QRS) . Then due to rapid efflux of K+ during repolarization. You’d see a much faster and more abrupt drop btwn phases 2 and 3 (a shortening of the Q-T interval and sharp peaked T wave)

92
Q

Hypokalemia (lowered K+) can result in

A

Tachycardia/arrhythmias

93
Q

How would less K+ (hypokalemia) influence the action potential and slope of the EKG

A

Hypokalemia will hyperpolarize cells and for cardiac cells they become hyperexcited. That slows repolarization and flattens out the T wave (sagging the ST segment)… also it elevates the U wave making it larger than the T wave

94
Q

What is the normal range of potassium in the blood

A

Between 3.7 and 5.2 mEq/L

95
Q

What can high amounts of calcium in the blood cause

A

Arrhythmias

Pathophysiology I - Exam 3 (Final) (5 decks)

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