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Cardio Pulm Eval > EKG Lecture > Flashcards

EKG Lecture Flashcards

1
Q

What 4 ions determine the electro-chemical gradient in cardiac cells?

A

K+
Na+
Ca++
Cl-

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2
Q

Resting membrane potential

A
  • 90 mV
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3
Q

Quick Review of Cardiac Action Potential

A

1) Simple two molecule systemwith semi-permeable membrane
2) Ion pump (Na-K ATPase) alters theconcentration of ions across membrane
3) An open K+ ion channel allows + charges to move out of the Compartment on the left, leaving behind relatively more negative charges

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4
Q

The resting membrane potential of cardiac muscle is primarily due to what ?

A

K+ equilibrium potential

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5
Q

Cardiac Muscle Action Potential

A
  • Wave of depolarization
  • Initially, only the K+ channels are open, so RMP = -90 mV
  • Depolarization of one part of the membrane (movement of + charge
    into the cell) spreads in a wave, causing voltage-gated Na+ ion channels in the adjacent membrane to spring open
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6
Q

What does the cardiac action potential depend on?

A

time-varying membrane conductance

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7
Q

What is QRS primarily caused by?

A

myocardial Na+ movement

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8
Q

T wave is the result of what?

A

myocardial K+ ion movement

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9
Q

What does ST segment mean as far as ion movement

A

no net movement
caused by Ca++

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10
Q

Refractory Period

A
  • During the Plateau phase (Phase 2 of the
    action potential) and during the first part of Phase 3, the
    myocardium cannot be stimulated again
  • During the later part of phase 3 and hyperpolarization, the
    myocardium can only be stimulated under abnormal conditions or with an extra impulse (ischemia, re-entrant currents, altered electrolytes
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11
Q

What is the state of the channels at rest

A

– K+ channels are open
– Na+ channels are closed
– eq potential = -90 mV

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12
Q

What is the state of the channels during depolarization

A

– K+ channels stay open
– Na+ channels open
– membrane potential= +30 mV

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13
Q

Is V4 positive or negative deflection

A

Depolarization is moving toward the electrode, producing a + deflection

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14
Q

Little block of ECG

A

1 vertical mm = 0.1 mV.
1 horizontal mm = 0.04 sec. (paper speed = 25 mm/sec)

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15
Q

Big Block of ECG

A

= 0.5 mV high
= 0.2 seconds long

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16
Q

Normal P-R Interval Time

A

0.12 - 0.2 s

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17
Q

normal QRS time

A

0.04- 0.1 s

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18
Q

normal Q-T time

A

0.32 - 0.40

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19
Q

Einthoven’s Triangle

A
  • Leads I, II, and III are bipolar with a + and - pole
  • Limb leads AVR (RA), AVL (LA), and AVF (LF)
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20
Q

Chest Leads

A
  • V1: 4th IC space R
  • V2: 4th IC space L
  • V3 : 1/2 way between V2 and V4
  • V4 : 5th IC space
    midclavicular line
  • V5 : 1/2 way between
    V4 and V6
  • V6: 5th IC space ant. axillary line
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21
Q

EKG Set up

A
  • first column: bipolar leads I, II, III
  • second column: unipolar limb leads avL, avR, avF
  • third column: unipolar chest leads
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22
Q

Conductions Path of Heart

A
  • From SA node, depolarization spreads to R and L atrium via inter- and intra- atrial tracts (Bachman’s bundle).
  • At AV node, conduction slows (P-R interval).
  • From AV node, depolarization spreads via the Bundle of His to the R & L Bundle branches (L anterior and posterior fascicles).
  • L & R bundles carry depolarization to Purkinje fibers.
  • Purkinje fibers spread depolarization to myocytes
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23
Q

what does Duration of P-R interval depend on?

A
  • Conduction velocity at AV node
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24
Q

What does QRS Complex Reflect?

A
  • Conduction through myocardium
  • Extensive branching
    and expansion of the
    wave of depolarization occurs via
    Purkinje’s fibers
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25
Q

What does the T wave represent?

A

left ventricle repolarizing in an organized manner

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26
Q

In what areas can a 12 lead EKG detect problems?

A

– heart rate
– heart rhythm
– hypertrophy (must be calibrated)
– infarction/ischemia (must be calibrated)

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27
Q

what do single lead EKGs detect?

A

rhythm and rate abnormalities

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28
Q

What cant telemetry detect?

A

hypertrophy or ischemia because it cant be calibrated

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29
Q

Systematic Evaluation of the EKG

A

1) P-wave: upright, before every QRS, always same
2) P-R interval: is it 0.12-0.2 s
3) QRS: all same, is it 0.06-0.10 s
4) T-wave: upright, normal
5) R-R interval: is it regular
6) HR: is it 60-100 bpm
7) Observe patient: does pt’s response to exercise
correlate with EKG?

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30
Q

Sinus Bradycardia

A

HR < 60 bpm.
– Normal in athletes (inc. SV)
– may occur with beta-blockers, Ca2+-channel blockers,
antiarrhythmic drugs or with vagal stimulation (vomiting or
suctioning)

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31
Q

Consequences of Sinus Bradycardia

A

dizziness, syncope, angina, diaphoresis

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32
Q

Sinus Tachycardia

A

HR > 100 bpm.
– caused by: fear, pain, exercise, caffeine, amphetamines,
nicotine, atropine, hyperthyroidism, hypoxia, CHF, fever

33
Q

Consequences of Sinus Tachycardia

A

usually benign

34
Q

What is Sinus Arrhythmia?

A
  • irregularity caused by SA node
  • often due to altered vagal stimulation
  • can be respiratory or non respiratory
35
Q

Respiratory Sinus Arrhythmia

A

increased heart rate with inspiration, decreased heart rate with expiration

36
Q

Causes of Non-Respiratory Sinus Arrhythmia

A
  • fever
  • infection
  • drug side effect or toxicity (digitalis and morphine)
37
Q

What do the chest leads indicated?

A

the axis of the heart (anatomic orientation of heart)

38
Q

What does left axis deviation suggest?

A

LV hypertrophy

39
Q

What does right axis shift suggest?

A
  • RV hypertrophy or MI
40
Q

What do you see on an EKG for RV hypertrophy

A

an increased R in V1

41
Q

What do you see on an EKG for LV hypertrophy?

A

Increased S wave in V1, increased R wave in V5

42
Q

How can ischemia be detected on an EKG

A
  • ST segment elevation
  • An inverted T wave or ST segment depression indicates acute ischemia
43
Q

What is happening in the heart between T and next cycles P wave?

A

passive ventricular filling

44
Q

What is occurring during the PR interval

A

atrial ejection

45
Q

what is occurring during QRS wave

A

isovolumic ventricular contraction

46
Q

what occurs during the ST segment

A

ventricular ejection

47
Q

Review Wiggers Diagram

A
48
Q

3 important determinants of CO

A
  • Preload
  • Afterload
  • Contractility
49
Q

Preload

A
  • volume with which ventricle is loaded
50
Q

what is preload determined by?

A

venous return and atrial kick

51
Q

Starling Law of the Heart

A

Greater stretch = greater force

52
Q

Afterload

A

resistance to blood flow

53
Q

what is the primary determinant of after load?

A

diastolic BP

54
Q

contractility

A

state of the cardiac muscle with regard to ability to generate force

55
Q

what happens to contractility with heart failure?

A

goes down

56
Q

what happens to contractility during acute and chronic exercise?

A

goes up

57
Q

how is contractility often measured?

A
  • with ejection fraction
  • Normal EF =50-75% (AHA, 2020), HF ≤ 40%
58
Q

What does the contractile state of the heart depend on?

A

intrinsic factors, the autonomic nervous system and hormonal states
– Intrinsic factors: training, disease, structure
– ANS: ACh (Vagus N.), Norepi. (Cardiac N’s)
– Hormonal factors: Epinephrine, Angiotensin and
other hormones

59
Q

What determines the level of activation of cardiac muscle?

A

Ca2+ influx

60
Q

what do drugs like calcium channel blockers, beta blockers, digitalis, etc affect

A

contractility by altering Ca delivery

61
Q

Effect of beta Adrenergic Stimulation

A

increased force, increased HR, increased relaxation rate

62
Q

Baroreceptor (cardiac reflexes)

A

– Carotid body sense increase in BP and alters vasodilatation, HR & contractility to normalize BP

63
Q

Bainbridge Reflex

A

R atrium senses increases in blood volume and modulates
HR (responsible for respiratory ECG rhythm)

64
Q

Chemoreceptor reflex

A

Brain stem senses CO2, H+ and O2 levels and alters HR, BP, contractility and respiration

65
Q

where is the primary sit of resistance

A

arterioles
- varies, depending on arterial vasomotor state

66
Q

Poiseuille’s Law

A

R= 8hl/pier4
For all practical purposes, R ~ 1 / r 4

67
Q

what are the two types of resistance in the body?

A

-Series: RT = R1+R2+R3 …
-Parallel: 1/RT = 1/R1+1/R2 +1/R3

68
Q

for the most part, what type of resistance is in the body?

A

parallel, so taking
away a R (such as in amputation of a limb) increases the total peripheral resistance (RT)

69
Q

what is radius of a blood vessel determined by?

A

– Local metabolic needs
– Vasoactive substances (adenosine, K+, H+, etc..)
– CNS (Sympathetic nervous system)
– Hormones: epinephrine (a1 receptors in vessels), angiotensin, antidiuretic H

70
Q

where does nutrient and waste exchange occur?

A

capillaries and venules

71
Q

two mechanisms of nutrient and waste exchange

A
  • Diffusion and Filtration
    – diffusion is most important for nutrient/waste
    – movement in to and out of tissues
    – filtration is most important for fluid balance
72
Q

Starling’s Hypothesis

A

depending of these forces, net filtration or absorption will occur

73
Q

What occurs to contractility and heart rate and resistance during acute exercise

A
  • HR and contractility increase
  • Resistance decreases
74
Q

what is the net effect of acute exercise on BP

A

SBP rises
Normal response: SBP increases to 130 or greater at max

75
Q

what occurs to BP if larger mutuel groups are exercised?

A

DBP either remains constant or decreases

76
Q

what occurs to BP if smaller mutuel groups are exercised?

A

DBP may increase slightly

77
Q

What does resistive exercise do to BP?

A

increases both SBP and DBP

78
Q

Abnormal responses of exercise on HR

A

– very rapid rise in HR:
* deconditioning or CV problem limiting SV
– little rise in HR:
* cardiac meds or heart disease
– decreased HR:
* severe disease and/or arrhythmia

Cardio Pulm Eval (10 decks)

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