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Advanced Life Support 2 (ALS2) > Chapter 4 Causes of cardiac arrest > Flashcards

Chapter 4 Causes of cardiac arrest Flashcards

1
Q

What is crescendo angina?

A

Angina on exertion, occurring with increasing frequency over a few days, provoked by progressively less exertion

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2
Q

What is stable angina?

A

Exertional chest pain that is relieved promptly with rest.

Does occur at rest

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3
Q

in unstable angina, the ECG may

A

Be normal
Show evidence of myocardial ischaemia (ST depression)
Non-specific abnormalities (TWI’s)

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4
Q

In patients with ACS but without chest pain, what is the predominant symptom?

A

Breathlessness

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5
Q

Other than chest pain, what are the features of aortic dissection?

A 
Hoarse voice
Swallowing difficulty
Back pain
Hypotension
Loss of a peripheral pulse/asymmetrical pulses
Neurologicial signs
Aortic murmur
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6
Q

A patient has acute chest pain, marked hypotension, no ECG evidence of AMI. What differential would you consider?

A

Aortic dissection

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7
Q

A patient has a good history and typical ECG evdience of a STEMI. Should you delay reperfusion to investigate further for PE or aortic dissection?

A

No. Only delay if there is strong evidence pointing towards these differentials.

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8
Q

How long do you have to provide PCI for a STEMI?

A

120 minutes

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9
Q

What has a worse prognosis: anterior, inferior or lateral infarction?

A

Anterior. Large area of left ventricle is damaged.

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10
Q

What vessel is occluded in an inferior infarction (II, III, aVF)

A

Right coronary artery (sometimes circumflex artery)

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11
Q

What vessel is occluded in a lateral infarction ( V5, V6, I, aVL)

A

Circumflex or diagonal of the LAD

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12
Q

What vessel is occluded in a posterior infarction?

A

Right coronary artery (circumflex in a left dominant person)

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13
Q

What are the ECG findings of a posterior infarction?

A

Reciprocal ST depression in anterior leads

Dominant R wave V1, V2 reflects posterior Q wave

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14
Q

What are of area of myocardium is affected in a posterior infarction?

A

Posterior LV

Posterior septum

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15
Q

How do you confirm a posterior infarction

A

Posterior ECG leads (V6, V7, V8, V7, V9, V10). Continuate around left axilla to the right of the spine

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16
Q

What type of/areas of infarction are at increased risk of ALSO having a right ventricle infarction?

A

1/3 of inferior and posterior STEMI’s involve the RV

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17
Q

How to use diagnose a right ventricle infarction?

A

May see STE in V1
Do right sided ECG (different to posterior ECG)
V1R to V6R leads added on
Suspect if patient has fluid responsive hypotension or raised JVP but no pulmonary oedema

18
Q

What ECG changes can be seen in SAH or traumatic brain injury?

A

Lots.

ST elevation, depression, TWI.

19
Q

Can troponin be elevated with PE, aortic dissection or myocarditis, chronic heart failure, chronic renal disease or acute sepsis?

A

yes

20
Q

How often is S1-QTIII (Dominant S wave in Lead I, Q wave + TWI lead III) seen in PE?

A

15%

21
Q

Is there benefit from reperfusion therapy after 12 hour?

A

Little to none. Can consider if ECG evidence of ongoing ischaemia.

22
Q

What is the common action of clopidogrel, ticagrelor and prasugrel?

A 
All block ADP receptor on platelets.
In STEMI
Clopidogrel 300 - 600mg or
Ticagrelor 180mg or
Prasugrel 60mg (not if > 75, < 60kg or hx bleeding or stroke)
23
Q

What are the indications for fibrinolysis?

A

Presentation within 12 hours of onset of chest pain suggestive of AMI, and:

  • ST elevation > 2mm in 2 adjacent chest leads or,
  • ST elevation > 1mm in 2 adjacent limb leads, or
  • Dominant R wave and ST depression V1 - V3 (posterior infarction)
  • New onset LBBB
24
Q

When giving fibrinolysis, what other drugs need to be given for treatment of STEMI?

A 
Aspirin 300mg
Clopidogrel 300 - 600mg (or ticagrelor 180mg)
Antithrombin therapy (enoxaparin or heparin or fondaparinux)
25
Q

What are the absolute contraindications to fibrinolysis?

A

1) Previous haemorrhagic stroke
2) Ischaemic stroke with 6 months
3) Central nervous system damage or neoplasm
4) Major surgery, head injury or other major trauma with 3 week
5) Active internal bleeding (menses excluded) or GI bleeding within past month
6) Known or suspected aortic dissection
7) Known bleeding disorder

26
Q

On the ECG what is suggestive of fibrinolytic therapy failure?

A

Failure of ST segment elevation to reduce by more than 50%

27
Q

What is ‘rescue angioplasty’?

A

PCI post fibrinolytic therapy.

Improves survival and reduces heart failure in those with failed fibrinolytic therapy

28
Q

What are the two immediate treatment outcomes in ACS?

A

1) prevent new thrombus formation

2) reduced myocardial oxygen demand

29
Q

How do you prevent thrombus extension in ACS?

A

Asprin
Clexane or heparin
And usually ADP receptor blocker if going for angiography

30
Q

How do you reduced myocardial oxygen demand?

A 
Beta blocker ( or non-dihydropyridine calcium channel blocker)
GTN +/- infusion if persistent pain
Consider early ACEI introduction

Treat heart failure or tachyarrhythmia promptly

31
Q

A patient has reperfusion therapy for ACS, then has an accelerated idioventricular rhythm. Does this require treatment?

A

No. Is usually transient and no treatment needed.

32
Q

What are bradyarrhthmias common with inferior infarctions?

A

Right coronary artery occlusion, loss of blood supply to SA and AV nodal arteries

33
Q

A patient has an inferior infarctin and develops heart block. What is the first thing you can to do treat them?

A

Atropine

34
Q

What is the only lead that looks directly at the right ventricle?

A

V1

35
Q

In a patient with inferior STEMI (RCA occlusion), what suggest a right ventricular infarction?

A

ST elevation in V1
ST elevation in V1 and ST depression in V2 (highly specific for RV infarction)
Isoelectric ST segment in V1 with marked ST depression in V2
ST elevation in III > II

Confirmed by presence of STE in right sided leads ( V3R, V6R)

36
Q

How many STEMIs are complicated by an RV infarction?

A

40%

Isolated RV infarction is rare though

37
Q

Why is diagnosing an RV infarction important?

A

They are very pre-load sensitive due to poor RV contractility.
Can develop severe hypotension in response to nitrates or other pre-load reducing agents.
Hypotension in RV infarction is treated with fluid loading. Nitrates contraindicated.

38
Q

A patient with ACS goes into cardiogenic shock. How would you treat?

A 
Consider frusemide (caution right ventriclular infarction)
BIPAP/ CPAP
Oxygen
Noradrenaline for vasopressor
Dobutamine as inotrope (B1 > B2 > Alpha)
39
Q

A patient with ACS develops cardiogenic shock. Do they have a good chance of surivial?

A

No. High mortality. May be reduced if urgent revascularisation provided.

40
Q

What are the electrical/ionopathies (ECG findings) that predispose someone to sudden cardiac death (predisposes to VF & VF)?

A

1) Long QT syndrome (inherited)
2) Acquired long QT
3) Brugada syndrome
4) Short QT syndrome (QTc < 340 + symptoms/syncope)
5) Catecholaminergic polymorphic ventricular tachycardia
6) Wolf-parkinson-White syndrome (risk of rapid AF transmitted to ventricles)
7) High grade AV block

41
Q

What are thy structural heart disease predisposing to suddent cardiac death?

A

1) Arrhythmogenic right ventricular cardiomyopathy (ARVC)
2) Hypertrophic cardiomyopathy (HCM)
3) Severe aortic stenosis
4) Dilated cardiomyopathy
5) Ischaemic/coronary heart disease
6) Anomalous coronary artery anatomy (congenital)
7) Other myocardial disease ( HTN, sarcoid, ect)

Advanced Life Support 2 (ALS2) (12 decks)

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