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EKG > midterm 2 > Flashcards

midterm 2 Flashcards

1
Q

what are we looking for with atrial hypertrophy

what would we see normally

A

look at V1
and II

normally you have a little cute P wave in II and a biphasic in V1

With RAH you have a peaked P in II and a peaked by in V1

with LAH you have a notched P wave in II and a negative biphasic wave in V1

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2
Q

what causes RAH (4)

A

pulmonary HTN
COPD
Tricuspid stenosis
congenital

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3
Q

what causes LAH

A

mitral stenosis

combined with LVH

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4
Q

Causes of LVH

A

aortic stenosis
mitral incompetence
HCM
HTN

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5
Q

criteria for LAH

A

Less than 1 box

notched P in I and II

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6
Q

criteria for RAH

A

greater than 1 small bok in V1 and

>2.5mm P in II

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7
Q

other than lead II where else would you expect to see a peaked p in a pt suspected of RAH

A

II AVF (all inferior)

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8
Q

lateral precordial and coronal leads

A

I

V5 and V6

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9
Q

RVH

A

V1–>V4

very large R wave
RAD in the is usually seen

usually you have a very small R with negative S in these leads

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10
Q

when attempting resuscitation of cardiac arrest what is not shockable

A

PEA asystole

only vtach and vfibb are shockable

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11
Q

how do you distinguish wandering pacemaker from MAT

A

MAT is wandering pacemaker over 100

remember we are seeing a P prime wave in all of these because it is not sinus paced

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12
Q

why do we see MAT

A

COPD or digitalis toxicity

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13
Q

no single impulse is depolarizing the atrium in this tachy that is seen with occasional impulse escape causing ventricle depolarization

A

A fibb

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14
Q

what is the increase in stroke associated with a fibb

A

fivefold

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15
Q

what is the increase in dementia associated with a fibb

A

twofold

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16
Q

what is the increase in heart failure associated with a fibb

A

threefold

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17
Q

what is the increase in deatg associated with a fibb for men/women

A

men 50%

women 100%

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18
Q

risk of developing a fibb in adults 40 and older

A

1/4 lifetime risk

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19
Q

supraventricular tachy associated with depolarization of 300-600 bpm

A

a fibb

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20
Q

why does a fibb occur

A

foci and frequency of ectopy increase with remodeling as fo electrical reentry

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21
Q

RF for Afibb

A 
obesity
 OSA
hyperthyroidism
diabetes
cardiomyopathy
heart failure
 LAE
excessive alcohol
and 
genetic predisposition

10!

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22
Q

sxs of a fibb (5)

A 
palpitations
dyspnea
fatigue
exercise intolerance
lightheadedness
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23
Q

MC physical exam finding for afibb

A

irregular and rapid pulse

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24
Q

other than irregular pulse what are some signs of a fibb

A

signs associated with heart failure
ischemic heart dz
and valvular heart dz

murmur, gallop, JVD, atrial bruits, crackles, hepatomegaly, peripheral edema,

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25
Q

how do we evaluate cardiac function and structure in a pt with afibb

A

TTE

transthoracic echocardiogram

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26
Q

what should we do for a pt that has had a fibb

A

ecg
tte
blood work (metabolic and thyroid panels)

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27
Q

how can you dx transient a fibb

A

ambulatory rhythm monitoring and mobile telemetry

can use trans esophageal echocardiograph (before cardioversion as this could cause embolus)

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28
Q

categories of a fibb

A

paroxysmal
persistent
longstanding persistent
permanent

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29
Q

what is paroxysmal A fibb

A

AF that terminated spontaneously or with intervention within 7 days and may reoccur with variable frequency

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30
Q

what is persistent A fibb

A

continuous AF (more than 7 days)

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31
Q

what is longstanding persistent a fibb

A

12 months

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32
Q

permanent a fibb

A

joint decision to stop trying

therapeutic attitude

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33
Q

two types of therapy for a fibb

A

rate control- sxs

rhythm control- for pts with sxs despite rate control

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34
Q

goal for rate control

and how do we achieve it

A

under 80 bpm
BB
non- dihydropyrodine CCB
(not in pts with HF)

digoxin adjunct to both of these

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35
Q

electrical cardioversion success for a fib

A

success 75-90%

returns 40-60% of the times
60-80% of pts in 12 months

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36
Q

success of antiarrythmic drugs for pts with a fibb

A

50%

37
Q

what is the most frequent site of AF electrical triggers and what kind of therapy targets them

A

MC cite is the pulmonary veins
can be targeted with transvenous catheter ablation

reoccurrence

38
Q

primary goal of AF managment

A

stroke prevention

39
Q

what is thought to be the reason for increased stroke risk

A

decreased blood flow velocity in the left atrial appendage

this allows for thrombus formation

40
Q

sxs of pericardial effusion

A

CP
SOB
DOE

feels better when you lean forward

41
Q

what is the most common EKG finding with pericardial effusion

A

low voltage QRS

42
Q

electrical alternans points to

A

cardiac tamponade

43
Q

what is electrical alternans

A

positively deflected QRS followed by low voltage amplitude

regularly irregular

44
Q

low voltage is defined as a peak to peak QRS amplitude of

A

<5mm in the limb and or <10 mm in precordial

45
Q

what causes low voltage EKG other than tompanade

A 
obesity
COPD
severe hypothyroidism
subcutaneous emphysema
massive MI
infiltrative/restrictive diseases such as amyloid cardiomyopathy
46
Q

what is beck’s triad

A

hypotension
JVD
muffled heart sounds

for cardiac tamponade and pericardiocentiusis

beck is eating a muffin with JVD and hypo

47
Q

ecg triad for cardiac tamponade

A

sinus tachy
low voltage
electrical alternans

48
Q

POCUS triad

A

point of care ultrasound

pericardial fluid
RV diastolic collapse
dilated IVC

49
Q

how to determine tahcy junctional rhythm

A

When assessing a rhythm strip for junctional tachycardia, look for a rate of 100 to 200 beats/min. The P wave is inverted in leads II, III, and aVF and can occur before, during (hidden P wave), or after the QRS complex.

50
Q

paroxysmal tachy rate range

A

150-250

51
Q

flutter rate range

A

25-350

52
Q

a fibb range

A

350-450

53
Q

3 pathophysiologies of a fibb

A
  1. dilation in intra atrial pressure leads to activation of RAAS and atrial remodeling and fibrosis
  2. disorganized electrical impulses develop usually originating from pulmonary veins
  3. left atrial squeeze is diminished LA appendage is stunned
54
Q

pathophysiology behind a fibb

A

larger number of ectopic sites can lead to fault atria and low CO or more commonly
atria do not empty completely into ventricles because

55
Q

sxs of A fibb

A 
palpitations 
tachycardia
DOE
fatigue
lightheadedness

but symptoms are absent in 1/3

56
Q

RVR

A

the heart rate is on average 150

57
Q

permanent af s also known as

A

longstanding persistent

58
Q

RF for AF

A 
OSA
Obesity
long standing HTN or CHF /heart dz
valvular heart disease 
cardiac surgery 
hyperthryoidism 
genetic predisposition
dehydrating factors: viral colonoscopy, cancer, alcohol
59
Q

what type of valvular disease are we likely to see leading to A fibb

A

left sided (mitral regurgitation and mitral stenosis)

60
Q

other than their pathophys origin how do AF stokes differ

A

more likely to reoccur and are often more fatal

61
Q

where do AF stroke occur

A

thrombus formation in the left atrial appendage

62
Q

what are the three treatment goals of Afibb

A
  1. prevent embolic stroke through anticoagulation
  2. prevent cardiac damage through heart rate control
  3. back to normal when necessary
63
Q

what is the stroke assessment?

A

CHADS2VASC score

also want to assess LV function and LA size and function?

64
Q

CHADVASC

A 
CHF
Hypertension
Age over 75 
Dm
Stroke
Vascular disease
Age between 64-75
Sex: female
65
Q

what medication should you be using based on a pts CHAD score

A

greater than 2 should be on . OACa

if 1 should be on OAC or ASA

66
Q

1 point stands for

A

clinically relevant non major

67
Q

2 point chad score stands for

A

clinically relevant risk factor major

68
Q

HASBLED stands for

A 
Hypertension
abnormal liver/renal
stroke
bleeding
labile INR
elderly >65
Drugs or alcohol
69
Q

which HASBLED criteria are worth 2 points

A

abnormal liver or renal
and drugs or alcohol

because they are two categories

70
Q

goal of anticoagulation therapy

A

to prevent embolic stoke by reducing thrombus burden in the heart LAA

71
Q

what is the go to anticoagulant for pts with AF

A

warfarin titrated to an INR 2-3

normal INR IS 1

72
Q

what do we use HAS-BLED for

A

Estimates risk of major bleeding for patients on anticoagulation to assess risk-benefit in atrial fibrillation care.

with a score of 3+ the pt is at increase risk of bleeding

need individualized approach

73
Q

Types of NOACs

A

Xa inhibitors

IIa inhibitors

74
Q

IIa inhibitors -name

A

dabigatran

75
Q

Xa inhibitors names

A

rovaroxaban
apixaban
edoxaban

76
Q

benefits of NOACs

what are the CI

A

no blood testing
no food interactions
less drug interactions
safer bleeding profile

contraindicated in mechanical heart valves/ severe mitral stenosis/ESRD

77
Q

how does Warfarin work

A

2,5,7,9

binds Ca and prevents the factors from forming a fibrin clot

(from fibrinogen to fibrin)

78
Q

which Xa inhibitor has low risk of bleeding and mortality benefit

A

eliquis (apixaban)

need to dose twice

79
Q

dabigatran pros and cons

A

direct thrombin IIa inhibitor

superior for ischemic CVA prevention
high risk for GI bleed and dyspepsia

80
Q

meds for rate control in AF

A 
BB 
bis
met
carve
neb

Non dihydropyrodine CCB (verapamil and dilitizem)

Digoxin for synergistic

last resort pacemaker

81
Q

when do we have to attempt rhythm conversion

A

in an unstable pt in emergent setting
when comorbidities have destabilized a pt (HF CAD pt with unstable angina)

thing of the algorithm unstable with a pulse

82
Q

when should you consider rhythm control (5)

A 
symtomatic AF despite rate control
difficult rate control
pts who have tachycardia mediated cardiomyopathy
younger active pts 
small left atrial size
83
Q

target HR in afibb

A

<110 is lenient
<80 is strict

need to titrate meds to lower rate based on symptoms with target being
70-90 is the range you want people to be in

84
Q

three types of rhythm control

A

electrical w/ TEE- echocardiogram of heart with a probe placed in the esophagus

Chemical cardioversion with amioderone
any medication has a toxic potential though

  1. transvenous catheter ablation- radio-frequency and cryotherapy on pulmonary veins (reoccurrence rate is 70-80%)
85
Q

what are we looking at with TEE

A

Atrial appendage

86
Q

what is the rules around stable rhythm conversion for a pt with a fibb as far as onset and treatment go

THERE IS A QUESTION ABOUT THIS

A

with onset unknown pt must be anti-coagulated fro 4 weeks prior

with onset known must occur within 48 hours and no TEE needed

87
Q

how would amiodarone be used

A

for rhythm control

high success and safe for all types of pts but can only be used for a short time due to EF

88
Q

how does a flutter treatment differ from AF

A

SVT re-entry tachy

use anticoagulation and rate control

rhythm control is considered early but doesn’t respond well to meds

atrial flutter ablation is typically much easier than AF (97%)

89
Q

what is the AF alogrithm

A

anticoagulation bassed hon HASBLED and CHADSVASC

rate control less than 110 to prevent heart damage

consider rhythm conversion based on continued symptoms and co morbidities

EKG (7 decks)

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