Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CVS > Acute Coronary Syndromes and Acute myocardial Infarction - Presentation And Investigation > Flashcards

Acute Coronary Syndromes and Acute myocardial Infarction - Presentation And Investigation Flashcards

1
Q

What are the different incidences of caridac chest pain?

New excertional angina?

Unstable angina?

Acute MI?

Sudden Cardiac Death?

A

New exertional angina - 52%

Unstable angina - 13%

Acute MI - 22%

Sudden cardiac death - 13%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is Stable Angina defined as?

A

Myocardial blood flow does not meet demand - ischaemia

Central chest tightness, often radiation to neck/arms

Aggravated by exertion & stress

Relief by stopping activity & rapid improvement with sublingual nitrate (GTN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the different acute coronary syndromes?

A

Unstable angina

NSTEMI

STEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does atherothrombosis formation (pathogenesis of all acute coronary syndromes) occur?

A

Plaque disruption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why do plaques rupture?

A

Inflammation and sheer stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the main difference between acute coronary syndromes and stable angina?

A

ACS - symptoms at rest

Stable angina - only on exertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the non-modifiable risk factors for Acute Coronary Syndromes?

A
  • Age
  • gender
  • creed
  • family history
  • genetic factors.
  • Previous angina
  • cardiac events or interventions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the modifiable risk factors for Acute Coronary Syndromes?

A
  • Smoking
  • Diabetes mellitus
  • Hyperlipidaemia
  • Hypertension
  • Lifestyle- exercise & diet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a typical history of unstable angina Pectoris (UAP)?

A

Angina on effort

Progressive increasing severity and frequency

Often provoked by less exertion or at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a typical history for those with NSTEMI?

A

Most often starts with myocardial ischaemic symptoms occurring at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the pain like in acute coronary syndromes?

A

Site - retrosternal

Character - often tight band/pressure/heaviness

Radiation - neck and/or into jaw, down arms

Aggravating factors - with exertion, emotional stress

Relieving factors - GTN, or physical rest; and/or ongoing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What must you ensure to check for on examination for unstable angina and NSTEMI?

A

HR, BP

Listen for murmurs, crackles in chest

May look very unwell

May look completely fine

Often no specific features to find

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the possible investigations for unstable angina and NSTEMI?

A

Electrocardiogram and Biomarkers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are common results of ECG in UAP and NSTEMI?

A

ECG results - often normal

Commonly ST-segment depression, transient ST-segment elevation and/or T-wave inversion

UAP - changes resolve after pain

NSTEMI - persist (but not always)

Serial ECGs to detect delayed changes essential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why is the difference in infarction between STEMI and NSTEMI?

A

STEMI - transmural

NSTEMI - sub endocardial infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do you differentiate between NSTEMI and unstable angina?

A

Biomarkers - troponin and CKMB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Here is why there is a rise in ST segment in STEMI

A

Rise in ST segment because:

Infarcted tissue loses the ability to maintain resting potential of -90mv. Sodium potassium pumps no longer work, so it is partially depolarised. Normally true baseline of an ECG is zero because there is no difference in voltage. However the positve vector of depolarisation travels away from the electrode - negative deflection of baseline – so it shifts lower. ST segment now appears elevated because the ST segment is where there is complete depolarisation – so the ST segment is on the true baseline. In comparison to original baseline, ST segment is higher up.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Here is why there is ST depression in NSTEMI

A

NSTEMI – depolarisation vector travels towards the detector, shift of baseline upwards. ST segment refers to the point where there is complete depolarisation. ST segment now appears lower. ST segment returns to normal because of fibrosis. Fibrotic tissue doesn’t have the ionic leakage of necrotic tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

When is there likely going to be an atypical ACS presentation?

A
  • Women
  • Elderly
  • Diabetics

Influenced by reduced pain sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the symptoms of angina and NSTEMI?

A

Breathlessness alone +/- signs of heart failure

Nausea & vomiting +/- other autonomic symptoms

Epigastric pain +/- recent onset indigestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does elevated cTn (cardiac troponin) suggest?

A

High risk of adverse events

Not all troponin elevations are ACS and caused by atherothrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does elevation of cardiac troponin indicate?

A

Elevated with compromise of myocyte integrity

Sensitive and specific marker of cardiac myocyte damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What do the levels of biomarkers indicate?

A

Characteristic rise and fall of cTn with ischaemic damage

Different pattern for acute myocardial infarction to UAP (unstable angina pectoris)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the immediate treatment for UAP and NSTEMI?

A

First ABCDE approach, then MONA

Morphine (or diamorphine)

Oxygen

Nitroglycerine (GTN spray or tablet)

Aspirin 300 mg orally (crush/chew)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What does antiplatelet therapy for UAP and NSTEMI event consist of?

A

Dual anti-platelet therapy (Aspirin & ADP receptor blocker) for one year following ACS event

(look at McClays pharmacology treatment of ACS and AMI for further details)

26
Q

What does antithrombotic therapy for UAP and NSTEMI consist of?

A

Intravenous unfractionated heparin (UFH) or s/c low molecular weight heparin (LMWH)

27
Q

What is other medical therapy for unstable angina and NSTEMI that isn’t anti-platelet therapy or antithrombotic therapy?

A

β-blockers recommended in ACS in absence of contraindications (asthma, acute left ventricular dysfunction, impaired AV nodal conduction)

  • Target HR between 50 and 60 bpm

Statins both acutely & chronically reduce further events.

ACE inhibitors: always if LV dysfunction, controversial if normal function

28
Q

Which UA/NSTEMI patients benefit from invasive strategy? (coronary revascularisation)

A

High risk patients

29
Q

Give examples of invasive strategy/ coronary revascularisation

A

Coronary angiography

Revascularisation by PCI

CABG

30
Q

What is the Typical Treatment Path for UA and NSTEMI (Not really in learning outcomes)

A

Most patients stay in hospital for 2-7 days.

Not all patients will have angiography, and not all who an angio. will need or have revascularisation.

Decisions more difficult in the elderly and/or those with important co-morbidities.

Many not reviewed after hospital discharge, some are for further decision making

31
Q

What is the result of coronary plaque rupture?

A

More complete, or complete thrombotic occlusion of coronary lumen and infarction of distal myocardium

Proximal occlusion of main artery causes greater damage

32
Q

What can the occlusion of distal or branch vessel cause?

A

If it supplies critical structure - significant problems

  • rupture of papillary muscle
  • acute mitral regurgitation
  • occlusion of AV nodal artery

CHB (complete heart block)

33
Q

What are the two forms of treatment for STEMI?

A

Fibrinolysis or primary PCI

34
Q

What is the effect of removing an occlusive thrombus early?

A

More myocardium will be salvaged.

Less LV damage results in better survival.

35
Q

Why is PCI better than fibrinolytic therapy?

A
  • Cardiac mortality
  • recurrent MI
  • reduced risk of haemorrhagic stroke
36
Q

When is PCI most effective?

A

Delivered within 120-150 mins of patient’s call for help (call to balloon time)

If door to balloon time is less than 90 minutes

If it has been over 3 hours of symptom onset

If there is cardiogenic shock, HF

High bleeding risk

If diagnosis is uncertain

37
Q

When is fibrinolysis the choice of treatment?

A

PCI cannot be performed

Door to balloon (of PCI) longer than 90 minutes

Symptoms present for less than 3 hours (PCI most effective between 120-150 minutes)

Difference between door to balloon is 1 or 2 hrs greater than door to needle

38
Q

When is the best time to initiate fibrinolysis?

A

Within 90 minutes of patient calling for help (call to needle) or within 30 minutes of hospital arrival

39
Q

How can call to needle be reduced?

A

Prehospital fibrinolysis

40
Q

What is the benefit of pre-hospital fibrinolysis?

A

Reduces early mortality by 15-20% in comparison to in-hospital fibrinolysis

41
Q

What are the risks of fibrinolytic therapy?

A

Increased risk of bleeding and intra-cranial haemorrhage in some patients

42
Q

Which patients have an increased risk of bleeding and intracranial haemorrhage?

A

Age > 75

Female

Previous stroke

Low body weight (F<65 kg, M<70 kg)

SBP > 160 mmHg

INR > 4 (international normalised ratio - how fast blood clots in patients receiving oral anticoagulant medication)

Chronic kidney disease & elevated creatinine

43
Q

What investigation would you use for STEMI for in-patient investigations?

A

Echocardiography

44
Q

What will echocardiography be used to see when examining a STEMI?

A

Size and nature of wall motion

Overal contractility

Presence and degree of mitral regurgitation

Presence of mural thrombus

45
Q

What are the most important determinants of MI survival?

A

Age

LV ejection fraction

46
Q

What percentage of sudden cardiac deaths are resuscitated and survive?

A

about 2%

47
Q

What is common in 80% of patients that are resuscitated & survive?

A

VT (ventricular tachycardia – life-threatening arrhythmia)

VF (ventricular fibrillation)

48
Q

Why does ACS result in ventricular arrhythmia?

A

Atherothrombotic event causes acute myocardial ischaemia and subsequent electrical disturbance

49
Q

Are all Sudden cardiac deaths ACS events?

A

NO

50
Q

What does sudden cardiac death look like on an ECG?

A
  • Irregular
  • Ineffective ventricular fibrillating activity
  • Multiple wavelets of electrical activity
51
Q

What is the only effective treatment for VF arrest?

A

Defibrillation

52
Q

How does sudden cardiac arrest differ from a heart attack?

A

Heart attacks - blockage in one or more coronary arteries, prevents heart from receiving enough oxygen-rich blood

Sudden cardiac arrest - electrical system to heart malfunctions and suddenly becomes very irregular

  • Heart beats dangerously fast
  • Ventricles may flutter or quiver (ventricular fibrillation) and blood is not delivered to body
53
Q

What does VF deteriorate into?

A

Asystole (heart stops beating)

54
Q

What is often proven to change the outcome of sudden cardiac death?

A

Bystander CPR

55
Q

What are the mechanical complications of MI?

A

Free wall rupture

Septal Wall Rupture

Papillary Muscle Rupture

56
Q

What are the ventricular arrythmia complications with MI?

A

VF

VT

57
Q

Describe another complication associated with MI than isn’t a mechanical or an arrhythmic complication?

A

LV Thrombus

58
Q

What is surgery for papillary muscle rupture or VSD?

A

Urgent surgery

Mitral valves replaced rather than repaired

VSD repair with pericardial or synthetic patch

Coronary artery bypass if needed & possible

If survive acute episode, long term prognosis is good

59
Q

How do you diagnose VF from an ECG?

A

P-waves and QRS complexes not present

Heart rhythm is highly irregular

HR is not defined (without QRS complexes)

60
Q

When is LV thrombus usually found?

A

48 hours after infarction

61
Q

What is treatment for LV thrombus?

A

Anticoagulation for 6/12 with warfarin and repeat echo

CVS (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions