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
What is 3rd degree AV block?
No action potentials from SA node pass through AV node
25
Describe the typical ECG appearance of 3rd degree AV block
P waves cause no QRS complex | Escape rhythms from ventricles - broad complex
26
How is 3rd degree AV block treated?
Ventricular pacing
27
What types of pacing options are available?
``` Transcutaneous - Emergency - Painful Transvenous - Via internal jugular/subclavian/femoral ```
28
When would a single chamber pacemaker be used?
Atrial - Isolated SA node disease Ventricular - AF with slow ventricular rate
29
What type of pacemaker is used in AV node disease?
Dual chamber
30
What are PVCs?
Broad complexes out with normal conduction
31
How are PVCs treated?
Beta blockers
32
How does VTach affect blood pressure?
Large sustained decrease
33
What kind of underlying pathology is present in VT?
``` Coronary artery disease Previous MI Cardiomyopathy LQTS Brugada syndrome ```
34
What is monomorphic VT and when may it occur?
Same QRSs arising from the same plane | Eg. From a post-MI scar
35
What is polymorphic VT and when does it occur?
Changing QRS complexes | Drug toxicity or Ischaemia in multiple areas
36
How is VT treated?
DCCV if unstable If stable - Pharmacological cardioversion - AADs
37
If we are unsure about a diagnosis of VT, what drug can be used?
Adenosine | No ECG change means it is likely VT
38
What is ventricular fibrillation?
Chaotic ventricular electrical activity
39
How is VF treated?
CPR Defibrillation 1mg IV adrenaline after 3rd shock (then every alternate shock) 300mg amiodarone
40
What is atrial fibrillation?
Chaotic atrial activity
41
What are the forms of the AF?
``` 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
What is lone/idiopathic AF?
AF in the absence of - Heart disease - Ventricular dysfunction
43
Where is the ectopic focus situated in AF?
Pulmonary veins (into LA)
44
ECG appearance of AF
Atrial rate >300bpm Irregularly irregular rhythm Ventricular rate - Variable
45
What are the treatment options for AF?
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
Torsades de Pointes appearance on ECG?
Long QT Wide QRS Changing QRS morphology
47
When are anticoagulants prescribed in AF?
``` In mitral valve disease In non-valvular AF - Age >75 - Hypertension - CCF - Previous CVA - CAD - Diabetes ```
48
What is atrial flutter?
Regular and rapid ATach Paroxysmal Sustained by macro-reentrant circuit in RA
49
AFlutter ECG appearance
Saw-tooth baseline
50
Treatment of AFlutter
RA ablation Drug therapy to lower ventricular rate DCCV Warfarin
51
What conditions does the term acute coronary syndrome encompass?
Unstable angina Acute NSTEMI STEMI
52
What is the history of an acute coronary syndrome?
``` Severe crushing central chest pain Radiation (arms and jaw) Prolonged Not relieved by - Rest - GTN Associated with - Sweating - Nausea - Vomiting ```
53
What ECG changes are noted in an MI?
ST elevation - first few hours T wave inversion - first day Q wave formation - After first day, indicate old MI
54
What conditions must be met for an MI to be classified as a STEMI?
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
What cardiac enzymes and protein markers may be high following an MI?
Creatine kinase | Troponin T
56
Treatment of an acute STEMI
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
When is PCI offered in an acute STEMI?
If available within 90 of contact
58
What is the alternative to PCI if it is unavailable/inappropriate?
Thrombolysis
59
Structural complications of MI
``` Cardiac rupture VSD MV regurgitation LV aneurysm Mural thrombus Pericarditis/Dressler's syndrome ```
60
Arrhythmic complications of an MI
VFib
61
Functional complications of an MI
LVF/RVF CCF Cardiogenic shock
62
What method of classification is used to calculate the risk of in-hospital mortality?
Killip classification
63
Symptoms of LVF
Dyspnoea (at rest and on exertion) Orthopnoea Paroxysmal nocturnal dyspnoea Po. oedema
64
Patient has tachycardia and a third heart sound. Fine basal crepitations are heard and a CXR shows alveolar bat wings and Kerley B lines.
Left ventricular failure causing pulmonary oedema
65
Patient presents with sacral oedema and a raised JVP. CXR is normal.
RVF
66
What is the standard treatment for LVF?
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
When initiating digoxin therapy, what needs to be monitored?
Serum levels roughly every 8-12hours
68
What are the six H's of reversible causes of cardiac arrest?
``` Hypovolaemia Hypoxia Hydrogen ions Hyper/Hypokalaemia Hypothermia Hypo/Hyperglycaemia ```
69
What are the six T's of potentially reversible causes of cardiac arrest?
``` Toxins Tamponade (cardiac) Tension pneumothorax Thrombosis (MI) Tromboembolism (PE) Trauma ```