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Adult Health 1 Review > T1 Blueprint - Cardiac Rhythm (Josh) > Flashcards

T1 Blueprint - Cardiac Rhythm (Josh) Flashcards

1
Q

What is the HR of Sinus Bradycardia?

A

less than 60 bpm

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2
Q

What are some causes of Sinus Bradycardia?

A

Increased Parasympathetic Tone (athletes)

SA Nodal disease (Sick Sinus Syndrome)

Meds

VAGAL STIMULATION

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3
Q

What is the hemodynamic effect of Sinus Bradycardia?

A

Decreased CO

Hypotension (orthostatic, syncope)

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4
Q

When do you treat Sinus Bradycardia and how do you treat?

A

ONLY if symptomatic

Use:

  • Atropine (DOC)
  • Pacemaker
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5
Q

What are the dysrhythmias we talked about?

A 
Sinus Brady
Sinus Tachy
Afib (most common)
Atrial Flutter
PACs
Junctionals (Accelerated Junctional, Junctional Tachy, PJCs)
SVTs
Ventricular Tachy
Vfib
PVCs
Heart Blocks
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6
Q

What HR is Sinus Tachy?

A

101 - 150 bpm

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7
Q

What are some causes of Sinus Tachy?

A

Increased O2 demand (fever, exercise)

Compensatory response to low CO (CHF, Dehydration, Hypovolemia)

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8
Q

What are the hemodynamic effects of Sinus Tachy?

A

increases the heart rate and improves CO

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9
Q

What do you do to treat Sinus Tachy?

A

correct the underlying cause

***ie: if fever, treat the fever

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10
Q

What is the most common dysrhytmia?

A

Afib

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11
Q

What is the rate associated with Afib?

A

greater than 350 bpm

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12
Q

What are some causes of Afib?

A

Heart Disease

Ischemia

Rheumatic Fever

Mitral or Tricuspid Valve disorders

Overstretched Atrium (HF)

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13
Q

What is the hemodynamic effects of Afib?

A

Lose Atrial Kick

Decreased SV

Decreased Diastolic filling time

CO can decrease by 20-30%

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14
Q

What are the three treatment goals of Afib?

A

Get them out of the Rhythm

Control the Rate (if you can’t get them out of the rhythm)

Prevent complications from Stasis of Blood

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15
Q

What is the number one fear associated with Afib?

A

stasis of blood in the Atrium

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16
Q

Afib:

What meds can be used to get them out of the rhythm?

A

Amiodarone

Ibutilide

Disopyramide

Flecainide

Dofetilide

Sotalol

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17
Q

Afib:

If meds don’t work, what else can we do to get them out of the rhythm?

A

Cardioversion

Surgical ablation (MAZE procedure)

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18
Q

Afib:

If you can’t get them out of the rhythm, what meds can we give to control the rate?

A

Ca Channel Blockers

Beta Blockers

Digoxin

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19
Q

What is the rate associated with Atrial Flutter?

A

250-350 bpm

***sawtooth appearance

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20
Q

With Atrial Flutter, will the client always know they have it?

A

No, because they may have a normal ventricular rate

***still lose their Atrial Kick

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21
Q

What are the Junctional Rhythms we talked about?

A

Junctional

Accelerated Junctional

Junctional Tachy

Premature Junctional Contraction (PJC)

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22
Q

What is a Junctional Rhythm?

A

AV Node takes over as pacemaker when a higher node fails to initiate or conduct to AV node

***rate is that of AV node (40-60 bpm)

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23
Q

What is the rate of a Junctional Rhythm?

A

40-60 bpm

***the normal rate of AV node

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24
Q

What do you use to treat a Junctional Rhythm?

A

Atropine

***If symptomatic

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25
Q

What is an Accelerated Junctional Rhythm?

A

Rate increases form normal junctional rhythm (40-60) to faster rate (61-100)

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26
Q

How concerned should we be about an Accelerated Junctional Rhythm?

A

not very concerned

no treatment necessary

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27
Q

What is Junctional Tachy?

A

rate faster than accelerated junctional

rate of 101-180 bpm

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28
Q

What is the Hemodynamic effect of Junctional Tachy?

A

Decrease CO due to abnormal atrial kick and rapid rate)

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29
Q

What is the medication mgmt for Junctional Tachy?

A

Ca Channel Blocker

Beta Blocker

Amiodarone

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30
Q

If meds don’t work, what can we do for Junctional Tachy?

A

AV Node ablation with pacemaker for severe, symptomatic patients

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31
Q

What happens with PJC?

A

Premature Junctional Contraction

  • single beat originating with AV junction that causes the atria to depolarize by retrograde conduction
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32
Q

What do we do about PJC?

A

just observe it

**It has no hemodynamic effect

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33
Q

What are some causes of PJC?

A

Irritable focuse within AV junction

Dig toxicity

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34
Q

When we think of Dig toxicity, what rate should we think of?

A

PJC

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35
Q

What is an SVT?

A

Supraventricular Tachy

  • any rapid rate originating above ventricle
  • Sinus tachy
  • Atrial tachy
  • Atrial flutter
  • Afib
  • Junctional tachy
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36
Q

What is the rate associated with SVT?

A

100-280 (with a mean of 170 in adults)

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37
Q

When do you treat SVT?

A

if it is paroxysmal (sudden onset)

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38
Q

What meds can be used for SVT?

A

Adenosine (Rapid Infusion)

Amiodarone

Cardizem

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39
Q

If meds don’t work, what else can be used for SVT?

A

Vagal Stimulation

Cardioversion

Ablation

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40
Q

What rate is Ventricular Tachy?

A

140-180 bpm

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41
Q

What do you do FIRST when you have Ventricular Tachy?

A

check pulse

  • **pulseless - defibrillator
  • **pulse - cardioversion
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42
Q

Treatment for PULSELESS Ventricular Tachy?

A

Defibrillator

CPR

Epi

Vasopressin

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43
Q

Treatment for Ventricular Tachy with a PULSE?

A

Amiodarone

Sotalol

Lidocaine

Cardioversion

44
Q

What is the concern with Vfib and Vtach?

A

can lead to Torsades

45
Q

What is the hemodynamic effect of Vtach?

A

No contraction

No forward blood flow

No CO

46
Q

What are the shockable rhytms?

A

Pulseless Vtach

Vfib

47
Q

How many jules for biphasic fibrillation?

Monophasic?

A

150-200j (requires less)

360j

48
Q

Management of Pulseless Vtach and Vfib?

A

Check for Pulse

(if no pulse) SHOCK

CPR for 5 cycles (about 2 mins)

Check for Pulse

49
Q

What does QRS look like with PVC?

A

wide and bizarre

can occur in bigeminey or trigeminy

50
Q

What is treatment for PVC?

A

Look for cause and treat it

  • Drugs
  • Hypoxia
  • Cardiac Disease
  • Irritation of ventricle by catheter

Antidisrhythmia meds

51
Q

Which Heart Block is hemodynamically stable?

A

1st Degree

52
Q

What do you do to treat 1st Degree Heart Block?

A

nothing, other than treating any possible cause

ex: if hyperkalemia, then get rid of some K+

53
Q

What are the different types of 2nd Degree Blocks?

A

Type I: Wenchenbach or Mobitz I

Type II: Mobitz II

54
Q

Which 2nd Degree Block is more severe?

A

Type II: Mobitz II

55
Q

What is hemodynamic effects of 2nd Degree Blocks?

A

stable but can progress to unsable

56
Q

If treating the underlying cause doesn’t correct 2nd Degree block, what else could be used?

A

possible transcutaneous pacing or transvenous pacing

57
Q

What is happening with the nodes during a Third Degree Block ?

A

each is firing at its own intrinsic rate (out of cycle)

58
Q

Which Heart Block is hemodynamically UNSTABLE?

A

3rd Degree

59
Q

Which Heart Block always requires pacemaker?

A

3rd Degree

60
Q

Which electrolyte determines conduction velocity and helps to confine pacing activity to the SA Node?

A

Potassium (3.5-5.0)

61
Q

What does Hyperkalemia do to electical system of heart?

A

Decreases rate of ventricular depolarization

Shortens Repolarization

Depresses AV conduction

62
Q

Potassium:

Acidosis is a sign of —

Alkalosis is a sign of —

A

Hyperkalemia

Hypokalemia

63
Q

What is treatment for Hyperkalemia?

A

D50W and IV Insulin (temporary)

Ca Chloride (temporary)

Cation exchange resin products into GI Tract such as Kayexalate (Permanent)

Hemodialysis or Peritoneal Dialysis (permanent)

64
Q

What doe Hypokalemia do to the electrical system of the heart?

A

impairs myocardial conduction

prolongs ventricular repolarization

***Hypokalemia reduces the excitability of cells so they are less responsive to stimuli

65
Q

What are some causes of Hyperkalemia?

A

Excess K+ administration

K+ sparing diuretics

ACE Inihibitors

ARBs

Renal Failure

Acidosis

Extensive Muscle Destruction (Rhabo)

66
Q

What are some causes of Hypokalemia?

A

GI Losses

Renal dysfunction

Alkalosis

Diuretic Therapy with insufficienty replacement

Chronic Steroid Therapy

67
Q

Treatment for Hyperkalemia?

A

K+ replacement (10 mEq per hr)

Replace magnesium if Hypomagnesium exists BEFORE replacing K+

68
Q

When replacing K+, how do we give?

A

Slowly (10 mEq per hr)

  • **High alert med
  • **Never IV Push
  • **Monitor for Phlebitis
69
Q

What is normal Magnesium level in ECF?

A

1.8-2.4 mg/dL

70
Q

Which is rare, Hypermagnesemia or Hypomagnesemia

A

Hypermagnesemia

71
Q

What are causes of Hypermagnesemia?

A

Renal dysfunction

Tumor Lysis Syndrome

Overtreatment w/ Mag

72
Q

Magnesium:

ECG for Hypermagnesemia looks similar to —

ECG for Hypomagnesemia looks similar to —

A

Hyperkalemia

Hypokalemia

73
Q

Hypomagnesemia and Hypokalemia both do what to the electrical function of heart?

A

Impair myocardial conduction

Prolong ventricular repolarization

74
Q

What are some causes of Hypomagnesemia?

A

Insufficient Mag intake

ETOH abuse

Diuresis / Diarrhea

Rapid administration of citrated blood products

75
Q

Magnesium

—- can lead to:

  • Sudden cardiac death
  • Coronary Artery spasm
  • HTN
  • Torsades
A

Hypomagnesemia

76
Q

Treatment for Hypomagnesemia?

A

Mag IV replacement

  • **evaluate renal status first
  • **Check for pulse

Pulseless = 1-2g in 10 mL D5W over 5-20 mins

Pulse = 1-2 g over 5-60 mins

77
Q

Which electrolyte is an important mediator for cardiac functions like vascular tone, myocardial contractility, and cardiac excitability?

A

Calcium

Total serum = 8.5-10.5 mg/dL

Ionized = 4-5 mg/dL

78
Q

What is difference between serum calcium and ionized calcium?

A

ionized is what you can actually use and represents that amount unbound to albumin

79
Q

Why would the following changes be associated with Hypercalcemia:

  • Shortened QTc Interval
  • Bradycardia
  • Heart Block
  • BBB
A

too much calcium:

  • Strengthens contractility
  • Shortens ventricular depolarization
80
Q

What are some causes of Hypercalcemia?

A

Bone Tumors

Hypomagnesemia

Endocrine Disorders

Excessive intake of Vit. D

81
Q

Treatment for Hypercalcemia?

A

Loop diuretics (Lasix)

Calcitonin (SQ or IM)

Bisphosphonates

Hemodialysis

82
Q

Why would the following be associated with Hypocalcemia:

  • Variable ECG
  • Bradycardia
  • Vtach
  • Asystole
  • Prolonged QT
A

too little calcium causes:

  • Decreased myocardial contractility
  • Reduced CO
  • Hypotension
  • Decreased responsiveness to Digoxin
83
Q

What are some causes of Hypocalcemia?

A

Post surgical blood loss (blood transfusions)

Alkalosis

Shock

Mag imbalances

84
Q

Treatment for Hypocalcemia?

A

Seizure precautions

Oral and IV replacement

  • Ca chloride
  • Ca gluconate
85
Q

12 Lead ECG:

What is Normal Axis?

A

Lead 1 = +

Lead aVf = +

86
Q

12 Lead ECG:

What is Right Axis?

A

Lead 1 = -

Lead aVf = +

87
Q

12 Lead ECG:

What is Left Axis?

A

Lead 1 = +

Lead aVf = -

88
Q

12 Lead ECG:

What is NW Axis?

A

Lead 1 = -

Lead aVf = -

89
Q

12 Lead ECG:

What causes Left Axis (+, -) Deviation?

A

Q waves of inferior MI

Emphysema

Hyperkalemia

Injection of contrast into Left Coronary Artery

Left Ventricular Hypertrophy

90
Q

12 Lead ECG:

What causes Right Axis (-, +) Deviation?

A

Normal finding in children and tall thin adults

Right Ventricular Hypertrophy

Chronic lung disease eve without pulmonary HTN

Anterolateral MI

PE

91
Q

12 Lead ECG:

What causes NW (-, -) Deviation?

A

Emphysema

Hyperkalema

Lead Transposition

Artificial Cardiac Pacing

Vtach

92
Q

12 Lead ECG:

What are the Limb Leads?

What are the Precordial Leads?

A

Limb = I, II, II, aVr, Avl, aVf

Precordial = V1, V2, V3, V4, V5, V6

93
Q

Which viewpoint of the heart do the Limb Leads provide?

A

frontal plane of heart

94
Q

Which viewpoint of the heard do the Precordial leads provide?

A

horizontal plane of the heart

95
Q

Where should V1 be placed?

A

4th ICS right sternal border

96
Q

What should we see in the R waves on the Precordial leads?

A

R Wave progression from V1 to V6

97
Q

When do you use Defibrillation?

A

NO PULSE

  • *Pulseless Vtach
  • *Vfib
98
Q

When do you use Cardioversion?

A

PULSE

  • *Afib
  • *SVT
  • *Vtach with a pulse
99
Q

Order with Defibrillation?

A

1) Check for Pulse
2) (if pulseless) Shock with 150-200 (if biphasic) or 360j (if monophasic)
3) Then 5 cycles of CPR (about 2 mins)
4) Check for pulse

100
Q

Cardioversion vs. Defibrillation:

Which is syncronized?

A

Cardioversion is synchronized because it needs to coincide with the PULSE

***Defibrillation is not synchronized because there is NO PULSE

101
Q

Pacemakers:

In the 3 code system, what do the following position means:

Position I

Position II

Position III

A

Position I = Chambers paced

Position II = Chambers sensed

Position III = Response to sensing

102
Q

Pacemakers:

What are the possible settings for Position I and Position II?

A 
0 = None
A = Atrial
V= Ventricle
D = Dual
103
Q

Pacemakres:

What are the possible settings for Position III?

A 
0 = None
T = Triggered
I = Inhibited
D = Dual (T and I)
104
Q

Pacemakers:

When we are pacing, what are we pacing?

A

A = Right Atria before P wave

V = Right Ventricle before QRS

D = both

105
Q

What are some indications for a Temporary Pacemaker?

A

Asystole

Pulseless idioventricular rhythm

Symptomatic brady that won’t respond to Atropine or Isuprel

Drug toxicity

Implanted pacer fail

106
Q

What are some containidcations for Temporary Pacemakers?

A

Prolonged cardiac arrest

Cardiac trauma

Extensive MI

107
Q

What are some complications from Pacemakers?

A

Catheter dislodgement

Lead failure

Pacemaker system failure

Erosion of pulse generator

Pacer induced tachy

Infection

Cardiac perforation with tamponade

Thrombosis or SVC

Dysrhythmias

Adult Health 1 Review (26 decks)

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