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Phase 2CARDIORESP > ECG Arrythmias > Flashcards

ECG Arrythmias Flashcards

1
Q

What is S1? When is it loudest?

A

Closure of the AV valves ie tricuspid and mitral loudest at mitral area

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2
Q

What is S2? When is it loudest?

A

Closure of the semilunar valves ie aortic and pulmonary Loudest at left upper sternal border

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3
Q

In terms of heart sounds, when is systole?

A

After S1, before S2 begins

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4
Q

When and where is S3 best heard?

A

•In early diastole during rapid ventricular filling phase •best heard at apex with patient in left lateral decubitus position.

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5
Q

What pathologies is S3 associated with? give 4

A

associated with increased filling pressure eg.

  1. Mitral regurgitation
  2. Aortic regurgitation
  3. Heart failure
  4. Thyrotoxicosis
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6
Q

What is S3 more common in anatomically?

Which groups is it normal in?

A
  • more common in dilated ventricles
  • Normal in age<30 yrs ie children, young adults, athletes and adults
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7
Q

When is S4 heard and where is it heard best?

A
  • In late diastole ie atrial kick
  • best heard at apex position with patinet in left lateral decubitus position
  • high atrial pressure
    *
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8
Q

What is S4 associated with?

A
  • associated with ventricular non-compliance eg hypertrophy
  • left atrium must push against stiff LV wall from LVH
  • therefore high atrial pressure
  • considered abnormal if palpable
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9
Q

What is a murmur?

A

Sound produced by turbulent flow of blood through heart, especially over abnormal valves

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10
Q

What is a thrill?

A

A palpable murmur

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11
Q

Which murmurs are louder on inspiration?

A

Right sided murmurs eg tricuspid regurgitation

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12
Q

Name the two subdivisions of slow heart rhythms ie bradyarrhythmias

A
  • Sinus Node Disease; treat if symptoms
  • HEART BLOCK; DANGEROUS; ALWAYS TREAT W OR W/O SYMPTOMS TO AID PROGNOSIS
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13
Q

What are fast heart rhythms ie tachyarrythmias divided into?

A

Supraventricular Tachycardias; not bad unless v fast

Ventricular Tachycardia; DANGEROUS

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14
Q

What are stops or pauses in sinus node disease?

A
  • flatline pauses
  • patient can block out
  • may also have seizure activity with pauses; lose control of bowels/bladder
  • but heart will restart
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15
Q

What is the most common ECG presenting feature of a PE?

A

sinus tachycardia

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16
Q

What is this finding?

A
  • Normal beats; flatline asystole
  • sinus pause because can see p waves
  • sinus arrest/block; sinus node is generating electricity but not getting it out
  • Failure of sinus node to fire or sinus exit block
  • may get dizzy; faint/asymptomatic
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17
Q

Give 3 treatment pathways for sinus node disease

A
  1. Conservative if asymtomatic
  2. Correct reversible causes eg electrolytes, drugs(beta blockers), thyroid function
  3. Pacemaker if remains symptomatic despite above steps
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18
Q

How does first degree heart block appear on an ECG?

A

Signal generated in SAN nad takes time to get into the AVN

  • Prolonged PR interval >200 msec
  • Benign and symptomatic; no treatment required
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19
Q

How many types of secondary AV block are there?

A
  1. Mobitz Type I; Wenckebach
  2. Mobitz Type II
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20
Q

What is Mobitz Type I?

A
  • Wenkebach
  • progressive lengthening of PR interval until a beat is dropped ie a p wave is not followed by a QRS complex
  • usually asymptomatic
  • Variable RR interval with a pattern ; regularly irregular
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21
Q

What is Mobitz Type II?

A
  • Dropped beats that are not preceeded by a change in the length of the PR interval as in type I
  • May progress to 3rd degree heart block; often treated with pacemaker
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22
Q

What is third degree heart block?

A
  • Complete heart block
  • atria and ventricles beat independently of each other
  • P waves and QRS complexes are not rhythmically associated
  • Atrial rate> ventricular rate
  • may be caused by Lyme disease
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23
Q

Describe the findings of this ECG and state the pathology

A

Prolonged PR interval (over 200 ms/5 small squares)

First degree heart block

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24
Q

Describe the findings of this ECG and state the pathology

A

4:1 Second degree heart block

Mobitz type II

after every 4 P waves there is a dropped QRS complex

PR interval in the conducted beats remains constant

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25
Q

Describe this ECG and state the pathology

A

Prolonged PR interval

First degree heart block

P wave is buried within the T wave

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26
Q

Describe the abnormalities in this ECG

A

PR is getting longer and longer after each beat and culminates in a dropped QRS interval

ie PR interval is longest immediately before the dropped beat

PR interval is shortest immediately after the dropped beat

MOBITZ TYPE I ie WENKEBACH second degree heart block

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27
Q

Describe the abnormalities in this ECG

A

Narrow QRS

P wave with long intervals then QRS then P wave

First T wave is pointier because it has a P wave in it.

No association between p waves and QRS complexes

Complete heart block

28
Q

What is percussion pacing and what is it used for?

A

A series of rhythmical blows to the chest to try and maintain circulation to the vital organs and try and enable a recovery of spontaneous trans-cutaneous or trans-venous pacing

Used in preference to CPR because it produces an adequate cardiac output with minimal external trauma

more likely to be successsful when ventricular standstill is accompanied by continuing P wave activity

29
Q

Give 3 treatment options for heart block

A
  • Conservative if asymptomatic and not high risk
  • Correct reversible causes eg drugs, electrolytes, thyroid function
  • Pacemaker; if symptomatic or high degree block
30
Q

What heart rhythms do pacemakers treat?

A

SLOW heart rhythms; ie do not treat fast heart rhythms; do NOT treat AF or regularise it.

31
Q

What should be done for safety before a pacemaker insertion?

A

Antibiotic Prophylaxis

32
Q

What is the main treatment for an MI

A

Take pt to cath lab and treat for primary PCI

33
Q

If a pt is bradycardic, has myocardial ischaemia/shock/hF/syncope, what should be done?

A

Give atropine 500 mcg IV

Then give atropine 500 mcg IV repeat to a maximum of 3 mg

OR do transcutaneous pacing

OR do isoprenaline 5 mcg/min IV

Adrenaline 2-10 mcg/min IV

34
Q

What can tachyarrhythmias be subdivided into?

A

Supraventricular Tachycardias

Ventricular tachycardias; DANGEROUS

35
Q

Describe this ECG

A

No P waves present

Fast AF NOT FLUTTER

There is

36
Q

Give 4 common causes of AF

A
  1. Obesity
  2. Hypertension
  3. Drugs esp alcohol
  4. Structural heart diseases; valves, congenital, cardiomyopathy

and also

endurance exercise/high vagal tone; seen in athletes

37
Q

What is the score used to assess the risk of having an ischaemic stroke with AF?

A

CHA2DS2-VASC

Congestive heart failure

Hypertension

Age>75

DM

Stroke/TIA in PMH

Vascular disease; prior MI

Age; 65-74

Sex; FEMALE

38
Q

When should you anticoagulate if there is AF?

A

If CHADS-VASC score is 2 or more

39
Q

Give 3 examples of rhythm control strategy

WHEN Should this be done?

A

DC cardioversion

Anti-arrhythmmic drugs

Ablation

done in young or symptomatic pts

40
Q

When should rate control strategy for AF be done? give 3 examples

A

If olderer, asymptomatic or little chance of restoring sinus rhythm.

  • Longstanding AF
  • Severe left atrial dilatation

Untreatable structural heart disease

41
Q

Vaughan Williams rate vs rhythm control drugs?

A

RHYTHM CONTROL:

  • Class I; Na channel blocker
  • Class III; Potassium channel blocker

RATE CONTROL:

Class II; Beta blocker

Class IV:Calcium channel blocker

42
Q

Describe the pathology seen in this ECG

A
  • 2 P waves for every QRS complex ie sawtooth pattern
  • Atrial flutter
  • poitiest going dowmwards
  • Broad QRS and LAD
  • V5 and V6 shows T wave inversion
43
Q

Define atrial flutter and compare it to AF

A

essentially the same causes as AF; lower stroke risk than AF

Lower risk of stroke than AF But higher than sinus rhythm

Anicoagulate w Atrial flutter if CHADSVASC is 2 or more

Harder to rate control than AF

Easier to cardiovert or ablate than AF

Atypical atrial flutter or atrial tachycardia is harder to ablate

44
Q

Describe this ECG

A
  • Fast rate of 150 bpm
  • SVT bc range is 140-280 bpm
  • Narrow QRS ie <120 ms usually
  • P waves are buried within
  • P waves only visible; retrograde conduction w inversion in leads ii,iii and avf
  • here the p waves are not visible. In V1 there is a probable P wave just after the QRS complex ie a retrograde p wave
45
Q

Describe the two types/causes of SVT

A
  • AVNRT; AV Nodal Re-entry Tachycardia; rapidly firing circuit within the AV node
  • AVRT; AV Re-entry Tachycardia; uses an accessory pathway ie a short circuit between atrium and ventricle and the AV node to make a circuit
  • accessory pathway is ablated in treatment
46
Q

Is AVNRT or AVRT more common?

What are the two directions of AVRT?

A

AVNRT is more common

AVRT can be:

  • ORTHODROMIC; going through the AV node in normal
  • ANTIDROMIC; going through the AV ndoe backwards
47
Q

How is SVT treated?

A
  • blocking the AV node with drugs terminates tachycardia because all the abnormal rhythms dpeend on the AV node for conduction therefore suppressing the AV node will stop abnormalities

Can use drugs;

  • Adenosine ( temporary fix of seconds)
  • Beta blocker
  • Calcium Channel Blocker

Also do DC cardioversion if compromised

48
Q

What is Wolff-Parkinson-White? (WPW)

A

Collection of clinical symptoms

need both tachyarrhythmias AND pre-excitation on ECG to be WPW

49
Q

What would you see on an ECG w WPW?

A

DELTA WAVE; slurring slow rise on the initial portion of the QRS/slurred upstroke;seen well on V4-V6

Short PR interval <120 ms; ie 3 small squares

WIDE AND ABNORMAL QRS complex

50
Q

What is this?

A

DELTA WAVE; Slurred UPSTROKE on QRS complex

51
Q

Why would you get antidromic AVRT in WPW?

A

If you conduct electricity through the pathway and it goes back up the AVN Backwards then you get broad complex tachycardia in WPW

will have a strong upsroke slur in QRS

Assume VT unless proven otherwise if a pt presents with this

52
Q

What is this?

A

ANTEDROMIC AVRT can see the delta wave

slurred upstroke in V6

Broad QRS bc antidomic

53
Q

How can WPW be cured completely?

A

Ablation

54
Q

What happens in AF from WPW?

A

AVOID BETA BLOCKERS AND ADENOSINE; WILL only speed up the accessory conduction pathway

  • Can give Amiodarone
  • Patient has gone into AF; because they have an accessory pathway in WPW, this conducts electricity faster than in the AVN
  • BROAD QRS, irregularly regular rhythm
55
Q

What are VENTRICULAR TACHYCARDIAS and ventricular fibrillation?

What can they cause?

WHICH can be more dangerous?

WHAT is the treatment?

A

Abnormal heart rhythm originating in the ventricles

cause palpitations, heart failure/syncope

VF is ALWAYS DANGEROUS>VT

Treatment= prompt defibrillation

Stable VT pts can be treated with drugs

OR most symptomatic patients with VF/VT may get a defibrillator

56
Q

What can you see in this ECG?

A
  • Broad QRS
  • No P waves, no T waves
  • BROAD COMPLEX TACHYCARDIA
  • Right Bundle Branch Block morphology; ie M shaped V1 and Wshaped QRS complex in V6
  • Probably coming from the left ventricle because left ventricle is being activated before the right
  • inferior leads; II and III and aVF can see the pointiest bit is pointed downwards; inferior STEMI
57
Q

What is Monomorphic Ventricular Tachycardia (VT)?

A
  • Usually caused by a scar in the ventricle
  • Most common cause is prior MI/ can be caused by scarring from other processes eg sarcoidosis, cardiomyopathy
  • May have cardiac output ( Pulse) ; this depends on the rate of VT and heart funcion
58
Q

Describe what you can see on this ECG

A
  • Polymorphic VT; TORSADES DE POINTES; QRS getting bigger and smaller in a wave like pattern
  • Completely flat baseline bc patient has just been shocked and defibbed; can see T wave inversion when patient goes into normal rhythm
59
Q

What is Polymorphic VT?

A
  • Torsades-de-pointes is a specifal case; Fast VT( 250-300 bpm) with a rotating QRS axis
  • usually caused by an ectopic beat in a vulnerable period ( R on T)
  • Usually no cardiac output
    *
60
Q

Give 4 causes of QT prolongation which could cause Polymorphic Ventricular Tachycardia

A
  • Long QT syndrome
  • Electrolyte abnormalities eg Low Ca/Mg/K)
  • Acute ischaemia
  • Bradycardia
61
Q

Describe the treatment for Polymorphic Ventricular Tachycardia

A
  • Often self-terminating; otherwise needs cardioversion with thump or DC shock
  • Tx: correcting cause and overdrive pacing
62
Q

Describe this ECG; is cardiac output present?

Give 4 causes of this pathology

Treatment?

A

VENTRICULAR FIBRILLATION; NO CARDIAC OUPUT

Causes: electrolyte abnormalities, myocardial acidosis, myocardial ischaemia eg current MI, ventricular scarring

Needs immediate defib or death will ensue

63
Q

EMERGENCY; ECG; with Broad QRS. DIfferentials and treatment for:

Regular rhythm

A
  1. Ventricular Tachycardia

Amiodarone 300 mg IV over 20-60 mins then 900 mg over 24 hours

  1. SVT with bundle branch block
    - Treat as for regular narrow complex tachycardia;

VAGAL MANOEUVRES

ADENOSINE 6 mg rapid IV bolus if no effect giving further 12 mg

64
Q

EMERGENCY TACHYCARDIA ECG ;BROAD QRS with IRREGULAR QRS

A
  1. AF with bundle banch block; treat as narrow complex AF ( Beta blocker)
  2. Pre-excited AF; consider Amiodarone
65
Q

EMERGENCY TACHYCARDIA WITH NARROW REGULAR RHYTHM TREATMENT?

A
  • Vagal manouevers
  • Adenosine 6 mg rapid IV bolus, give further 12 mg if needed
66
Q

NARROW QRS TACHYCARDIA WITH IRREGULAR RHYTHM TREATMENT?

A
  • Probable AF; control with beta blocker or dilitiazem
  • If in heart failure, consider digoxin or amiodarone
  • assess thromboembolic risk and consider anticoagulation

If atrial flutter control with beta blocker

Phase 2CARDIORESP (11 decks)

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