Lecture 1 Flashcards

1
Q

DEF: Analgesia

A

The diminution or elimination of pain

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2
Q

DEF: Conscious Sedation

A

Minimally depressed state of consciousness that:

  • Retains ability to independently maintain airway and
  • Respond appropriately to stimuli/commands
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3
Q

DEF: Minimal Sedation

A

Minimally depressed state that:

  • Retains ability to independently maintain airway
  • Respond normally to tactile/verbal stimulation
  • Cardio unaffected
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4
Q

DEF: Moderate Sedation

A

Pt responds PURPOSEFULLY to verbal commands

  • Retains ability to maintain airway
  • Cardio usually maintained
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5
Q

DEF: Deep Sedation

A

Pt cannot be easily aroused
BUT responds purposefully to REPEATED or PAINFUL stimuli
- May not be able to maintain airway- may need assistance
- Cardio usually maintained

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6
Q

DEF: General Anesthesia

A

Pt not arousable, even w/ painful stimuli

  • Independent airway often impaired- require assistance via positive pressure ventilation
  • Cardio function may be impaired
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7
Q

Enteral Administration Types

A

Oral, Sublingual, Rectal

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8
Q

Parenteral Administration Types

A

IM, IV, IN, Inhalation, submucosal, subcutaneous, intraosseous
- Bypass GI tract

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9
Q

Heart orientation in chest

A
  • Rotated 30 deg to the left lateral side

- R. Ventricle is most anterior

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10
Q

Tricuspid Valve

A

Between R. atrium and R. ventricle

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11
Q

Mitral Valve

A

Between L atrium and L ventricle

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12
Q

Normal heart’s “pacemaker”

A

Sinoatrial Node

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13
Q

Normal Cardiac Conduction Pathway

A

SA Node–> AV Node –> Bundle of HIS–> splits left and right here–> Purkinje Fibers –> to cardiac muscle cells

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14
Q

Intrinsic Rate of SA Node

A

60-100 bpm

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15
Q

Intrinsic Rate of AV Node

A

40-60 bpm

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16
Q

Intrinsic Rate of Bundle of His

A

40-60 bpm

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17
Q

Intrinsic Rate of Purkinje Fibers

A

20-40 bpm

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18
Q

If SA Node fails to initiate an impulse, what happens?

A

AV Junction (Consists of AV Node and Bundle of His) takes over as the pain pacemaker and heart rate will have a rate of 40-60 bpm

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19
Q

Characteristics of AV Junction as the Pacemaker

A
  • Rate of 40-60 bpm

- Rhythms have a missing or inverted P-Wave!

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20
Q

What if both SA Node and then AV Junction fail??

A

The ventricles will fire impulses themselves at a rate of 20-40 bpm

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21
Q

What is the effect on the QRS complex of the heart relying on the ventricles for the pulse rather than the SA node or AV Junction?

A

QRS complex will be wide - >120ms

Normal is 80-120ms

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22
Q

AKA “fast response AP’s”

A

Non-Pacemaker AP’s

Have rapid depolarization

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23
Q

AKA “slow response AP’s”

A

Pacemaker AP’s
Have slow depolarization
Found in SA and AV nodes

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24
Q

Opening of what channels start depolarization in Non-Pacemaker cardiac cells

A

Na Channels

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25
Opening of what channels start depolarization in Pacemaker Cells
Ca Channels
26
Which cardiac cells have a true resting membrane potential and what is it?
Non-pacemaker cells | -90 mV
27
Explain the Non-pacemaker cell AP graph
Phase 4 - resting potential at -90mV due to K leaving cell--> Cell gets rapidly depolarized to -70mV--> Phase 0 - Rapid depolarization - Fast Na channels open and K channels close --> membrane potential gets more positive Phase 1 - Initial repolarization due to opening of transient K channels Phase 2 - Plateau phase- due to L-type Ca channels still open -- prolongs AP Phase 3 - K channels open and Ca channels close allowing full repolarization back to Phase 4
28
Non pacemaker cell Phase 1
Initial repolarization due to opening of transient K channels which cause short-lived hyperpolarization
29
Non pacemaker cell Phase 0
Depolarization caused by opening of Fast Na channels at -70 L Ca channels also open at -40 and K channels close
30
Non pacemaker Phase 2
Plateau phase - due to L Ca channels still open--> causes plateau
31
Non pacemaker Phase 3
Opening of K channels and closing of L Ca channels--> Repolzarization
32
Non pacemaker Phase 4
-90 mV - most negative - due to K channels open and K leaving cell
33
AP in Non-pacemaker cells primarily determined by what channels
Fast Na channels, L type Ca channels, and K conductance
34
Depolarizing current in SA node AP's carried by what ion?
Slow Ca currents
35
Explain the Pacemaker cell AP graph
Phase 4 - spontaneous depolarization up from -60 to -40 due to funny currents of slow inward Na, then T Ca channels open, then L Ca channels open--> until action potential reached around -40 (K channels close too) Phase 0 - Depolarization! Primarily via L Ca channels Phase 3 - Repolarization - via K channels openning and L Ca channels closing
36
Pacemaker cell Phase 0
Depolarization! Via L Ca channels!
37
Pacemaker cell Phase 4
K channels closing, Funny currents from slow Na inward, then T Ca channels open, and the L Ca channels open further depolarizing until reached AP threshold
38
Pacemaker cell Phase 3
Repolarization due to K channels opening and L Ca Channels closing
39
AP in Pacemaker cells primarily determined by changes in which Ion conductance
Ca and K
40
Hyperkalemia effect on cardiac rate
Bradycardia!!
41
DEF: Preload
The end diastolic volume in the left and right ventricles The stretching of the muscle cells to their extend after passive filling and then atrial contraction and right before ventricular contraction
42
DEF: Afterload
The pressure in the left venticle during ejection- essentially the load against which the heart ejects blood The greater the aortic pressure, the greater the afterload
43
DEF: Normal Sinus Rhythm
60-100 bpm Each QRS preceded by normal, upright P wave QRS complexes
44
Draw out normal sinus rhythm
__--__v^v__^___
45
Causes of longer duration QRS
Hyperkalemia | Bundle Branch Block
46
DEF: P Wave
Depolarization of the atria
47
DEF: PR Interval
Time it takes for electrical impulse to get from SA node thru the AV node Normal: .12-.20 sec
48
DEF: QRS Complex
Rapid depolarization of the ventricles | Normal: 0.08-.12 sec
49
DEF: T Wave
Repolarization of the ventricles
50
DEF: QT Interval
Depolarization and Repolarization of the ventricles | Normal:
51
Effect of Myocardial Ischemia on EKG
Depression of ST segment or | Flattening or inverting of T wave
52
Effect of STEMI on EKG
ST segment elevation
53
DEF: METs
Metabolic Equivalents of Tasks 1 MET is 3.5mL of O2 per kg of body weight Must be able to meet 4 METs to climb a flight of stairs or walk two blocks BASICALLY a measure of ability to complete daily tasks
54
METs
Can't climb flight of stairs | At greater risk of cardiovascular problem
55
Someone with METs
Administer less Epi? | Make sure don't have quick or large changes in pulse or BP
56
DEF: Ejection Fraction
% of blood leaving heart each time it contracts
57
Normal Ejection Fraction
55-70%
58
Evidence of Systolic Heart Failure
Ejection Fraction
59
DEF: Baroreceptor Reflex
Homeostatic mech to maintain BP
60
How does Baroreceptor Reflex work?
Provides a negative feedback loop--> if senses elevated BP, it sends signal to heart to decrease rate so as to dec BP A dec in BP causes dec baroreceptor activation and thus causes heart rate to inc due to lack of signals from baroreceptor Baroreceptor slows down HR by activation or Parasymps and Inactivation or Symps
61
Baroreceptor locations
Aortic arch and carotid sinus
62
Drug eluting vs. Bare metal stent
Drug eluting stents release drug to reduce restenosis
63
Use of anti-platelet therapy with Drug eluting vs bare metal stents
Okay to treat bare metal stent pt 1 mo after placement if only on aspirin. Have to wait 6 mo to a year for drug eluting to take only aspirin
64
What provides innervation to the heart?
Vagus N.
65
Parasympathetic predominance on heart leads to
Slowing the HR
66
Parsympathetics on the Heart
Release Ach--> goes to Muscarinic receptors--> opens K channels--> slows heart depolarization
67
Sympathetic predominance on the heart leads to
Increasing the HR
68
Sympathetics on the Heart
Release NE and E --> goes to B1 receptors--> opens Na and Ca channels--> inc rate of depolarization --> Inc HR
69
Parasympathetics use which receptors on heart?
Muscarinic
70
Sympathetics use with receptors on heart?
B1