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Year 1 - Cardiovascular (DP) > Acute Myocardial Infarction > Flashcards

Acute Myocardial Infarction Flashcards

0
Q

What factors oppose filtration out of capillaries?

A

pic - Capillary osmotic pressure

Pi - Interstitial fluid hydrostatic pressure

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1
Q

What forces favour filtration of substances out of capillaries?

A

Pc - Capillary hydrostatic pressure

pii - Interstitial fluid osmotic pressure

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2
Q

What is the equation for net filtration pressure?

A

NFP = (Pc + pii) - (pic + Pi)

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3
Q

At which end of the capillary is NFP positive, which end is negative, and why is this useful?

A

Positive - Arteriole (Favouring filtration - oxygen and ions out)
Negative - Venule (Favouring absorption - carbon dioxide in)

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4
Q

What are common mechanisms of oedema?

A 
Raised capillary pressure
- Arteriole dilation
- Increased venous pressure - LVF/RVF
Decreased plasma osmotic pressure
- Malnutrition
- Malabsorption
Lymphatic insufficiency
Changes in capillary permeability
- Histamine
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5
Q

Characteristics of supraventricular arrhythmias?

A

Narrow QRS

Originate above ventricles

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6
Q

Characteristic of ventricular arrhythmias?

A

Broad complex

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7
Q

Examples of supraventricular arrhythmias?

A 
Supraventricular tachycardia
Atrial fibrillation
Atrial flutter
Ectopic atrial tachycardia
Sinus bradycardia
Sinus pauses
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8
Q

Examples of AV node arrhythmias?

A

AV node re-entry
Accessory pathway
AV block

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9
Q

Examples of ventricular arrhythmias?

A

Premature ventricular complexes
Ventricular tachycardia
Ventricular fibrillation
Asystole

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10
Q

What are some autonomic causes of arrhythmia?

A 
Sympathetic stimulation
- Nervousness
- Exercise
- CCF
- Hyperthyroidism
Increased vagal tone
- Bradycardia
- Heart block
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11
Q

How does temperature affect automacity?

A

Hypothermia
- Decreased phase 4 pacemaker slope
Hyperthermia
- Increased phase 4 slope

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12
Q

What other factors increase the phase 4 slope of the pacemaker AP?

A 
Hypoxia
Hypercapnia
Cardiac dilation
Local Ischaemia
Hypokalaemia
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13
Q

How many an afterdepolarisation during phase 3 occur?

A

Digoxin toxicity
Torsades de Pointes
- Long QT syndrome
- Hypokalaemia

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14
Q

Common symptoms of arrhythmia?

A 
Palpitations
SoB
Syncope
Sudden cardiac death
Worsening of pre-existing condition
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15
Q

Arrhythmia investigations

A 
12 lead ECG
CXR
Echo
ETT
24 hr Holter
Event recorder
EP study - Induce and study arrhythmia
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16
Q

How can atrial ectopics be treated?

A 
Beta blockers
Avoid stimulants (caffeine and cigarettes)
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17
Q

When may sinus bradycardia be physiological/expected?

A

In an athlete
Patient using beta blockers
Patient with an inferior STEMI

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18
Q

Treatment of sinus bradycardia

A 
Atropine
Pacing if haemodynamically unstable
- Hypotension
- CCF
- Angina
- Collapse
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19
Q

Treatment of SVT

A 
Acute
- Vagal manoeuvres/Carotid massage
- IV adenosine
- IV verapamil
Chronic
- Avoid stimulants
- Radiofrequency ablation
- Antiarrhythmic drugs (Beta blockers [class ii] or Calcium channel blockers [class iv])
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20
Q

What is first degree AV block and how is it treated?

A

PR interval >0.2s

Long term follow-up

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21
Q

What is second degree AV block type I?

A

Progressive PR lengthening
Eventual cropped beat
Vagal origin

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22
Q

What is second degree AV block type II?

A

Always pathological
X number of P waves until a QRS
- eg. 3 P waves per QRS is a 3:1 block

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23
Q

What treatment is indicated in 2nd Degree type II block?

A

Permanent pacemaker

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24
Q

What is 3rd degree AV block?

A

No action potentials from SA node pass through AV node

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25
Q

Describe the typical ECG appearance of 3rd degree AV block

A

P waves cause no QRS complex

Escape rhythms from ventricles - broad complex

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26
Q

How is 3rd degree AV block treated?

A

Ventricular pacing

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27
Q

What types of pacing options are available?

A 
Transcutaneous
- Emergency
- Painful
Transvenous
- Via internal jugular/subclavian/femoral
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28
Q

When would a single chamber pacemaker be used?

A

Atrial
- Isolated SA node disease
Ventricular
- AF with slow ventricular rate

29
Q

What type of pacemaker is used in AV node disease?

A

Dual chamber

30
Q

What are PVCs?

A

Broad complexes out with normal conduction

31
Q

How are PVCs treated?

A

Beta blockers

32
Q

How does VTach affect blood pressure?

A

Large sustained decrease

33
Q

What kind of underlying pathology is present in VT?

A 
Coronary artery disease
Previous MI
Cardiomyopathy
LQTS
Brugada syndrome
34
Q

What is monomorphic VT and when may it occur?

A

Same QRSs arising from the same plane

Eg. From a post-MI scar

35
Q

What is polymorphic VT and when does it occur?

A

Changing QRS complexes

Drug toxicity or Ischaemia in multiple areas

36
Q

How is VT treated?

A

DCCV if unstable
If stable
- Pharmacological cardioversion
- AADs

37
Q

If we are unsure about a diagnosis of VT, what drug can be used?

A

Adenosine

No ECG change means it is likely VT

38
Q

What is ventricular fibrillation?

A

Chaotic ventricular electrical activity

39
Q

How is VF treated?

A

CPR
Defibrillation
1mg IV adrenaline after 3rd shock (then every alternate shock)
300mg amiodarone

40
Q

What is atrial fibrillation?

A

Chaotic atrial activity

41
Q

What are the forms of the AF?

A 
Paroxysmal
- Lasts less than 48 hrs
- Often recurrent
Persistent
- Lasts >48 hrs
- Can still be cardioverted to NSR
- Unlikely to spontaneously cardiovert
Permanent
- Inability to cardiovert by all means
42
Q

What is lone/idiopathic AF?

A

AF in the absence of

  • Heart disease
  • Ventricular dysfunction
43
Q

Where is the ectopic focus situated in AF?

A

Pulmonary veins (into LA)

44
Q

ECG appearance of AF

A

Atrial rate >300bpm
Irregularly irregular rhythm
Ventricular rate
- Variable

45
Q

What are the treatment options for AF?

A

Initial rate control therapy
- Beta blocker OR rate-limiting Calcium channel blocker
- Digoxin (in paroxysmal AF in sedentary patients)
If monotherapy does not control symptoms
- Dual therapy of any two of beta blocker, calcium channel blocker and digoxin

If rate control therapy has not worked

  • Offer Amiodarone for 4 weeks before DCCV
  • Transoesophageal/Convential DCCV
  • Continue amiodarone for 12 months after DCCV

Offer left atrial ablation in paroxysmal and persistent AF

46
Q

Torsades de Pointes appearance on ECG?

A

Long QT
Wide QRS
Changing QRS morphology

47
Q

When are anticoagulants prescribed in AF?

A 
In mitral valve disease
In non-valvular AF
- Age >75
- Hypertension
- CCF
- Previous CVA
- CAD
- Diabetes
48
Q

What is atrial flutter?

A

Regular and rapid ATach
Paroxysmal
Sustained by macro-reentrant circuit in RA

49
Q

AFlutter ECG appearance

A

Saw-tooth baseline

50
Q

Treatment of AFlutter

A

RA ablation
Drug therapy to lower ventricular rate
DCCV
Warfarin

51
Q

What conditions does the term acute coronary syndrome encompass?

A

Unstable angina
Acute NSTEMI
STEMI

52
Q

What is the history of an acute coronary syndrome?

A 
Severe crushing central chest pain
Radiation (arms and jaw)
Prolonged
Not relieved by
- Rest
- GTN
Associated with
- Sweating
- Nausea
- Vomiting
53
Q

What ECG changes are noted in an MI?

A

ST elevation - first few hours
T wave inversion - first day
Q wave formation - After first day, indicate old MI

54
Q

What conditions must be met for an MI to be classified as a STEMI?

A

Greater than 1mm ST elevation in 2 adjacent limb leads
Greater than 2mm ST elevation in at least 2 contiguous precordial leads
Possibly new onset BBB

55
Q

What cardiac enzymes and protein markers may be high following an MI?

A

Creatine kinase

Troponin T

56
Q

Treatment of an acute STEMI

A

MONA-C

  • 5mg IV morphine/diamorphine (+ anti-emetic eg metoclompramide)
  • High flow oxygen (If hypoxic)
  • Nitrates (GTN if BP>90mmHg)
  • 300mg oral Aspirin
  • 300mg oral Clopidogrel
57
Q

When is PCI offered in an acute STEMI?

A

If available within 90 of contact

58
Q

What is the alternative to PCI if it is unavailable/inappropriate?

A

Thrombolysis

59
Q

Structural complications of MI

A 
Cardiac rupture
VSD
MV regurgitation
LV aneurysm
Mural thrombus
Pericarditis/Dressler's syndrome
60
Q

Arrhythmic complications of an MI

A

VFib

61
Q

Functional complications of an MI

A

LVF/RVF
CCF
Cardiogenic shock

62
Q

What method of classification is used to calculate the risk of in-hospital mortality?

A

Killip classification

63
Q

Symptoms of LVF

A

Dyspnoea (at rest and on exertion)
Orthopnoea
Paroxysmal nocturnal dyspnoea
Po. oedema

64
Q

Patient has tachycardia and a third heart sound. Fine basal crepitations are heard and a CXR shows alveolar bat wings and Kerley B lines.

A

Left ventricular failure causing pulmonary oedema

65
Q

Patient presents with sacral oedema and a raised JVP. CXR is normal.

A

RVF

66
Q

What is the standard treatment for LVF?

A

Initially
- Low does loop diuretic (Furosemide)

If patient has hypertension/angina
- Consider Amlodipine

Consider anticoagulants if history of thromboembolism

Second line (specifically for LVF)

  • Low dose (titrated) ACE inhibitor
  • Beta blocker (once patient is no longer acute)
  • Consider an ARB if patient has a dry cough

If patient is intolerant of ACEi and ARB
- Consider Hydralazine + nitrate

Seek specialist advice before prescribing
- Aldosterone antagonsist (Spironolactone or Eplerenone)

If first and second line treatments do not control symptoms

  • Digoxin
  • ICD
67
Q

When initiating digoxin therapy, what needs to be monitored?

A

Serum levels roughly every 8-12hours

68
Q

What are the six H’s of reversible causes of cardiac arrest?

A 
Hypovolaemia
Hypoxia
Hydrogen ions
Hyper/Hypokalaemia
Hypothermia
Hypo/Hyperglycaemia
69
Q

What are the six T’s of potentially reversible causes of cardiac arrest?

A 
Toxins
Tamponade (cardiac)
Tension pneumothorax
Thrombosis (MI)
Tromboembolism (PE)
Trauma

Year 1 - Cardiovascular (DP) (6 decks)

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