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Cardiopulmonary PT > Abnormal EKG > Flashcards

Abnormal EKG Flashcards

1
Q

What leads go with the lateral, anterior, septal, and posterior part of the heart?

A

Lateral: I, aVL, V5, V6
Anterior: V3, V4
Septal: V1, V2
Inferior: II, III, aVF

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2
Q

You see a EKG with a normal looking rhythm, and you notice there is a P wave for every QRS and a T wave is present. What is the rhythm?

A

Normal sinus

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3
Q

What is sinus arrhythmia?

A

THe QRS complexes are not equidistant from each other.

Will have some variability because when we breathe in our HR increases and when we breathe out our HR decreases. But too much variability is a bad thing

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4
Q

Who has sinus bradycardia and what are the symptoms?

A

Normal in athletes, beta blockers cause this, decreased function of the SA node causes this.

Asymptomatic unless pathological condition exists (presence of 2 or 3 degree heart block)

Dizziness, syncope, angina

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5
Q

T/F: low blood flow is a risk factor for dementia or Alzheimer’s?

A

True

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6
Q

What are causes of sinus tachycardia?

A 
Fear
Anxiety
Caffeine
Nicotine
Amphetamines
Demands of O2 are higher (exercise, infection, MI, hemorrhage)
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7
Q

What are causes and symptoms of sinus tach?

A

Generally benign
SA node automaticity increased
Patients asymptomatic

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8
Q

T/F: PAC is a block in the conduction of impulse from SA node to atria?

A

False: sinus exit block

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9
Q

On an EKG you see a normal rate (~70) and you notice that after a T wave there is a pause equal to 2 complete cardiac cycles before the next P wave. What is the rhythm?

A

Sinus exit block

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10
Q

Do patient with sinus exit block have symptoms?

A

These blocks are less than a second so they are usually asymptomatic. BUT if they complain of SOA or other symptoms you may need to contact someone

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11
Q

What are causes of PAC? Symptoms? Possible consequences?

A

Causes: emotional stress, nicotine, caffeine, alcohol, infection, hypoxemia, MI, atrial damage

Symptoms: asymptomatic and if frequency is low no treatment required and pt should be able to participate in activity

If frequency increases a tach or a fib may result.

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12
Q

What is a rhythm where the P wave comes quick after the T wave and is a little more peaked?

A

Premature atrial contraction: ectopic focus in either atria initiates an impulse before the next impulse initiated by the SA node

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13
Q

What are some causes for atrial tachycardia?

A

PAC, pulmonary HTN, altered pH, COPD

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14
Q

What are symptoms of a tach?

A

Q compromised if prolonged: dizziness, fatigue, SOB

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15
Q

What does a tach look like on an EKG?

A

R-R very close together.
HR may be 100-200 bpm
Hard to make out P wave (blends with T)

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16
Q

What are causes of A flutter?

A

Mitral valve disease, CAD, infarction, stress, renal failure, pericarditis, rheumatic heart disease, MI

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17
Q

What are symptoms of A flutter?

A

Unless ventricular rate becomes too high Q is not compromised.
So patients are asymptomatic.
In their chart you may see: uncontrolled, controlled, with symptoms, w/o symptoms (uncontrolled means R waves are coming faster and rate is not as normal)

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18
Q

What are characteristics of A flutter?

A

Saw tooth P waves
R-R interval is normal
What’s happening is there is a rapid firing of ectopic source in atria and the AV node is blocking the signal from getting to the ventricles.

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19
Q

What is A fib?

A

Erratic quivering of atria: multiple ectopic foci, no true depolarization, AV node acts to control ventricles

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20
Q

What are causes of A fib?

A

Advanced age, CHF, ischemia or infarction, cardiomyopathy, digoxin toxicity, drug use, stress/pain, renal failure

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21
Q

WHat are consequences of Afib?

A

puts patient at risk for stroke because blood is sitting in the atria and it gets sticky and clotted. The clot will be at risk for moving and traveling to the brain

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22
Q

What are problems associated with Afib?

A

No atrial kick: accounts for 30% of Q so in a fib Q will be compromised

If rate is 100 bpm at rest: monitor assessed during all activities and engaged with caution (likely to have Q decompensation)

23
Q

T/F: in both a fib and a flutter it’s easy to make out the P wave?

A

False: in a fib it’s hard to make out the P wave

24
Q

You are looking at an EKG and you see that there is an immediate QRS after a T wave and it is missing a P wave. What is this rhythm?

A

Premature junctional contraction

25
Q

You are looking at an EKG you see QRS complexes but no P waves and you notice the rate is very slow. What is the likely rhythm?

A

Junctional escape rhythm

26
Q

What are causes of junctional escape rhythm and what are symptoms?

A

Causes: increased vagal tone, digoxin toxicity, infarction, severe ischemia to conduction system (R CAD)

Decreased HR= low Q, results in sx of dizziness, fatigue. will have symptoms with mobilization

Will be candidates for pacemaker or meds to increase HR

27
Q

What happens to SA node in junctional escape rhythm?

A

Not functioning properly.

AV junction takes over and ventricular rate is between 40-60 bpm

28
Q

What are causes of PVCs?

A

Caffeine, nicotine, stress, overexertion, electrolyte imbalance, ischemia, cardiac disease, CHF, over distension of ventricle, acute infarction, irritation of myocardium or vessels, chronic lung disease and hypoxemia

29
Q

What are symptoms of PVCs?

A

May have symptoms if more frequent or more serious in nature.
Decreased Q for that heart beat.
Patient activity can be compromised.
Exercise should be monitored if patient having isolated or couplet PVC

30
Q

What is sequelae if there are increased frequency of PVCs?

A 
Filling time is decreased
Decreased pre load
Decreased SV
Decreased Q (dizzy, SOB)
Can lead to v tach
31
Q

What are the types of PVC?

A 
Unifocal: one part of ventricle
Multifocal: coming from two different places in ventricle
Couplet
Run
Bigeminy
Trigeminy
32
Q

What are causes of V tach?

A

Ischemia, acute infarction, hypertensive heart disease, reaction to meds

33
Q

What are symptoms of V tach?

A

Q and BP diminished

Symptoms: light headed, syncope, weak thread pulse, disorientation

34
Q

What is V fib?

A

Sequel to v tach
Life threatening
Emergency
Shockable rhythm

35
Q

What is a idioventricular rhythm?

A

No p wave
wide QRS
Ventricle is pacing: 20-40 bpm
Will convert to systole because the rate is not sustainable for long due to decreased cardiac output

36
Q

What are causes of first degree heart block?

A

CAD, infarction, reaction to digoxin

37
Q

What are symptoms of first degree heart block?

A

asymptomatic unless rate

38
Q

What are causes and symptoms of second degree heart block type 1?

A

Cause: right CAD or infarction, digoxin toxicity, excessive beta blocker

Benign arrhythmia; generally asymptomatic (no sx and sufficient Q)

39
Q

What are causes and symptoms of second degree heart block type 2?

A

Cause: MI (especially LAD), ischemia/infarction of AV node, digoxin toxicity

Symptomatic when HR is low and Q compromised

40
Q

What are causes and symptoms of third degree heart block?

A

Cause: acute MI, digoxin toxicity, degeneration of conduction system

Sx: if slow HR, Q is diminished; pt may complain of dizziness, SOB, possibly angina

Medical emergency

41
Q

What does a pacemaker rhythm look like?

A

A properly functioning pacemaker will show a sharp spike, followed immediately by depolarization of the chamber it is intended to pace. This rhythm strip shows ventricular pacemaker capturing every beat. Note absence of mappable P waves and sharp spikes followed immediately by wide QRS complexes.

42
Q

How do you determine LVH?

A

Add mm of height of S wave in V1 or V2 with R wave in V5 or V6

If sum is >35 mm OR/AND R wave in aVL is >11 mm you have LVH

43
Q

How do you determine if you have RVH?

A

If R wave is bigger than S wave in V1 and gets smaller through precordial leads you have RVH

Remember that normally the R wave increases from V1-V6

44
Q

T/F: From V1-V6 the S wave gets smaller?

A

True

45
Q

What signifies LAE?

A

Broad p wave in lead II (sometimes seen in I and aVL)

OR/AND

Diphasic p wave in V1 with larger terminal component

46
Q

What signifies RAE?

A

Peaked pointy p wave in lead II (sometimes III, V1, aVF) which is greater than or equal to 2.5mm

47
Q

what are injury patterns seen in EKG?

A

Injury: elevated ST segments greater than 1 mm

Ischemia: symmetrical T wave inversion >3 mm in two adjacent leads

Infarct: Q waves that are at least 0.04 seconds wide or 1/3 of entire QRS in height

48
Q

What are changes in EKG at each stage of MI?

A

Acute stage: ST elevation
Hours: ST elevation, decreased R wave, Q wave begins
Day 1-2: T wave inversion, Q wave deeper
Days later: ST normalizes, T wave inverted
Weeks: ST and T normal, Q wave persists

49
Q

What are locations onf the heart of the leads?

A

II, III, aVF: inferior LV, RA, LA

I, aVL: high lateral LV

V1, V2: RV, RA, LA, anteroseptal LV

V2-V4: anterior and apical LV

V4-V6: anterolateral LV

50
Q

Where will you see the BBB?

A

Right BBB in V1, V2
Left BB in V5, V6

Right BBB: more M shaped
Left BBB: bat man hat

51
Q

Why are there two R’s in a BBB?

A

There is a delay with a signal so one side will fire before another causing two waves.

So in left BBB: R is the right ventricle firing and R’ is the left ventricle firing (flip this if there was a right BBB)

52
Q

What conditions are seen our acute cardiac patient population?

A 
Cardiopulonary insufficiency
CP sequelae of surgery
CP sequelae of restricted mobility
Cardiac conditions: post MI, CABG
Deconditioning/bed rest
53
Q

What is EBP for cardiac patients and exercise (chronic heart failure and CV disease)?

A

Guidelines similar to older adults:
FITT
Study had participants do five 40 min ex sessions per week at 60-70% HRR. They found exercise was well tolerated, they increased distance walked, VO2 peak, and QOL. But they found long term adherence was a barrier

54
Q

What is clinical decision making model for cardiac patients?

A

1) Identify all factors contributing to deficits in O2 transport
2) Determine whether mobilization and ex are indicated and which specifically address O2 deficits.
3) Match appropriate mobilization/ex to patient’s O2 transport capability
4) Set intensity within therapeutic and safe limits of pt O2 transport.
5) Post surgical- combine upright position with thoracic mobility; active or AAROM, breathing control
6) Set duration to pt response vs. time
7) Increase intensity, duration or both as pt tolerates w/o distress
8) Continue to progress until functional status improves or until threat of O2 transport is minimized

Cardiopulmonary PT (19 decks)

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