B4.001 Tachycardia Big Case Flashcards

1
Q

what is intermittent ventricular fibrillation?

A

doesn’t exist

you can’t spontaneously recover if you have ventricular fibrillation

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2
Q

what is tachycardia

A

rhythm with 3 consecutive beats > 100bpm

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3
Q

what are some mechanisms for tachycardia

A

enhanced automaticity
re-entry
triggered beats

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4
Q

what is atrial fibrillation?

A

most common form of sustained arrhythmia

atria out of coordination with ventricles

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5
Q

risk factors for a-fib

A

5% of people older than 65
2:1 M:F
lifetime risk for 40 yo is 1 in 4

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6
Q

different types of a-fib manifestations

A

paroxysmal

persistent

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7
Q

why can a-fib be deadly?

A

blood can pool in left atrium due to ineffective pumping and eddy formation
blood that is stagnant can develop clots, particularly in the L atrial appendage
induce a 4-5x increased risk of ischemic stroke

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8
Q

associations with a-fib

A

organic heart disease (electrical or mechanical)

disturbances of sympathetic-vagal balance (endocrine, physiological)

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9
Q

possible contributors to a-fib

A
anxiety
anemia
reactive hypoglycemia
herbal supplement toxicity
drugs
alcohol abuse
coronary disease
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10
Q

if you recognize a-fib in a patient, what do you do in response?

A
  1. call cardio for a consult, hopefully within 24 hrs
  2. CBC, TSH, electrolytes, LFTs and fax to cardio
  3. abstain from possible contributors
  4. begin anticoagulation therapy
  5. start rate control therapy
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11
Q

what are the 4 big parts of managing a-fib

A
  1. ECG in all pts
  2. anticoag unless contraindicated
  3. initial rate control with beta-blocker or Ca channel blocker (digoxin only as adjunct)
  4. transthoracic echo in most (transesophageal only when it changes management)
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12
Q

why would you want a transesophageal echo?

A

left atrial appendage visualization

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13
Q

what is cardioversion

A

administering a shock to regulate sinus rhythm

atria receive smaller shock than ventricles

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14
Q

what is ablation?

A

a procedure that can correct heart rhythm problems (arrhythmias)
works by scarring or destroying tissue in your heart that triggers or sustains an abnormal heart rhythm
in some cases, ablation prevents abnormal electrical signals from entering your heart and, thus, stops the arrhythmia

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15
Q

3 ways to increase cardiac output

A

increase HR (electrical adjustment)
increase power behind beats (muscle power adjustment)
fix “sloppy” valves, streamline efficiency

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16
Q

how does HR respond to exercise?

A

increases consistently with level of activity

17
Q

how does SV respond to exercise?

A

lowest when standing
slight increase with activity, but much less than HR
increase with sitting and laying down as well

18
Q

describe the conduction velocities at different locations in the heart

A
vary greatly between areas
AV node = 0.05 m/sec
atrial muscle = 0.5
ventricular muscle = 0.5
bundle of His = 2
left and right bundles = 2
Purkinje fibers = 4
19
Q

where is conduction velocity the lowest

A

AV node

20
Q

what is the direction of conduction through the heart

A
SA
atrial muscle
AV
bundle of HIs
left and right bundle branches
Perkinje fibers
ventricular muscle
21
Q

what creates the P wave on an EKG

A

atrial depolarization

22
Q

what creates the QRS complex

A

heart contraction due to opening of voltage gates Na channels

23
Q

which ions are depolarizing

A

Na

Ca

24
Q

which ions are repolarizing

A

K

25
Q

difference between SA/AV vs atrial/ventricular action potentials

A

SA/AV
-no resting potential
-funny sodium currents responsible for phase 0 depolarization (open during repol)
atrial/ventricular
-resting potential present
-voltage gated sodium currents responsible for phase 0 depolarization

26
Q

CO =

A

HR * SV (l.ventricle)

27
Q

PBF =

A

HR * SV (r.ventricle)

28
Q

in general, how do left and right ventricular stroke volumes compare?

A

generally the same since HR is the same on each side and CO = PBF

29
Q

MAP =

A

CO * TPR