Brainscape's Knowledge GenomeTM

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


See full index

Systems: Cardiovascualar AB > AMI- Presentation and Investigation > Flashcards

AMI- Presentation and Investigation Flashcards

1
Q

What are the 4 most common presentation of coronary heart disease in the community?

A
  • New exertional angina
  • Acute MI
  • Unstable angina
  • Sudden cardiac death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Stable angina

A

If myocardial blood flow is reduced with increased demand then ischaemia occurs

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

What is the classic presentation of stable angina?

A

Central chest tightness often with radiation to neck and/or arms

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

What are aggravating factors of stable angina?

A
  • Exertion

- Stress

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

What are relieving factors for stable angina?

A
  • Stopping activity

- Rapid improvement with sublingual nitrate

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

What causes stable angina?

A
  • Fatty streak becomes a non-obstructive plaque

- When it becomes an obstructive plaque >70% obstructed then stable angina occurs

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

What process is responsible for stable angina?

A

Atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

When do acute coronary syndromes occur?

A

When there is spontaneous plaque rupture and local thrombosis with degrees of occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does plaque rupture lead to?

A

Plaque disruption leads to atherothrombosis formation

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

What 3 conditions make up ACS?

A
  • Unstable angina
  • NSTEMI
  • STEMI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is atherothrombosis caused by?

A

Unstable plaques

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

What type of plaques result in stable angina?

A
  • Fibrous plaque

- Atherosclerotic plaque

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

Why do plaques rupture?

A

-Inflammation is important determinant in plaque stability, along with other mechanisms including shear stress

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

What is the main difference between the presentation of ACS and stable angina?

A

ACS symptoms will almost always give symptoms at rest in contrast to stable angina which is only on exertion

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

When taking a history, why is it important to establish the characteristics of the patients pain?

A

To differentiate from other causes of chest pain

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

What is the history of pain relating to ACS?

A
  • Retrosternal pain
  • Character is tight band/pressure/heaviness
  • Radiates to neck and/or jaw and/or down arms
  • Aggravated by exertion, emotional stress
  • Relieved by, incomplete improvement with GTN or physical rest, remain ongoing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the non-modifiable risk factors for coronary artery disease?

A
  • Age
  • Gender
  • Creed
  • Family history
  • Genetics factors
  • Previous angina, cardiac events or interventions
  • Race
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the modifiable risk factors for coronary artery disease?

A
  • Smoking
  • Diabetes mellitus
  • Hyperlipidaemia
  • Hypertension
  • Lifestyle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Unstable angina pectoris

A

Angina on effort, but of progressive increasing frequency and severity often provoked by less exertion and/or then at rest

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

NSTEMI

A

Starts with myocardial ischaemia symptoms occurring at rest

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

Examination of unstable angina and NSTEMI.

A
  • May look very unwell
  • May look completely fine
  • Often no specific features to fins
  • Ensure you check HR, BP, murmurs and crackles in the chest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ECG of unstable angina and NSTEMI.

A

May be normal but:

  • Commonly ST depression, transient ST elevation and/or T wave inversion
  • More often in UAP changes resolve after pain and in NSTEMI they tend to persist
  • Serial ECGs to detect delayed changes is essential
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is important to remember when making a diagnosis of UAP or NSTEMI?

A
  • Typical symptoms are not always present in ACS cases

- Atypical ACS presentation is more often seen in women: the elderly or diabetics, influenced by reduced pain sensation

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

What are some atypical symptoms of UAP 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
25
Q

What is the main biomarker used in UAP and NSTEMI?

A

-Cardiac troponin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Why is troponin useful to look at when making a diagnosis?

A
  • Helpful in risk stratification
  • Elevated cTn suggest 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
27
Q

What is cardiac troponin?

A

Contractile apparatus of myocytes thin filaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

When is cardiac troponin elevated?

A

With compromise of myocyte integrity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is troponin a marker of?

A

Cardiac myocyte damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

When does myoglobin peak after AMI?

A

<0.5 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

When does cardiac troponin peak after AMI?

A

1-2 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

When does CK-MB peak after AMI?

A

Around 1 day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

When does cardiac troponin peak after UAP?

A

Around 1 day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the immediate treatment for UAP and NSTEMI?

A
  • ABCDE approach

- Followed by MONAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the MONAC approach?

A
  • Morphine
  • Oxygen
  • Nitroglycerine
  • Aspirin (300mg orally)
  • Clopidegrol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What anti-platelet therapy should all ACS patients receive?

A

Both aspirin and a ADP receptor blocker such as clopidegrol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What anti-thrombotic therapy should ACS patients receive?

A

IV unfractionated heparin or low molecular weight heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the advantages of low molecular weight heparin?

A
  • Improved clinical outcome
  • Easier to administer
  • Given subcutaneously
  • Does not need to be monitoredd
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What other medications should ACS patients be put on?

A
  • B blockers
  • Statins
  • ACE Inhibitors
40
Q

Why is coronary revascularisation considered?

A

Clear evidence that high risk patients with UA/NSTEMI benefit from early invasive strategy compared to medical therapy alone

41
Q

What types of coronary revascularisation are available?

A
  • PCI

- CABG

42
Q

What is the treatment path for UA and NSTEMI?

A
  • Most patients stay in hospital for 2-7 days
  • No all patients will have angiography and not all who have it will have revascularisation
  • Decisions more difficult in the elderly and/or those with important co-morbidities
  • Many not reviewed after hospital discharge
43
Q

Why are STEMIs more severe?

A
  • Plaques rupture leads to more complete, or complete thrombotic occlusion of coronary lumen and infarction of distal myocardium
  • Proximal occlusion of main artery causes greater damage
  • However, occlusion of distal or branch vessel which supplies critical structures can cause significant problems (rupture of papillary muscle, acute mitral regurgitation, occlusion of AV node artery)
44
Q

What occurs in a time dependent manner following STEMI?

A

Necrosis of myocardial tissue

45
Q

What increases the amount of cardiac tissue that can be salvaged?

A

The sooner the occlusive thrombus is dissolved/removed and the vessel opened

46
Q

What results in better survival of a STEMI?

A

Less LV damage

47
Q

What are the choices in how to open infarct related artery?

A
  • Fibrinolysis

- Primary PCI

48
Q

Why is primary PCI considered superior over fibrinolysis?

A
  • Reduces mortality
  • Reduces recurrent MI
  • Reduced risk of haemorrhagic stroke
49
Q

When is PCI most effective?

A

Between 120-150 minutes after event

50
Q

What is the treatment of choice for STEMI when PCI cannot be performed?

A

Fibrinolytic therapy

51
Q

When is fibrinolytic therapy most effective?

A

Within 90 minutes of event or 30 minutes on arrival to hospital

52
Q

What does fibrinolytic treatment increase the risk of?

A

Bleeding and intra-cranial haemorrhage in some patients

53
Q

Who is at increased risk of bleeding with firbrinolytic therapy?

A
  • Age>75
  • Female
  • Previous stroke
  • Low body weight
  • SBP>160mmHg
  • INR>4
  • Chronic kidney disease and elevated creatinine
54
Q

What treatment is used as secondary prevention treatment for STEMI?

A

-General measures (stop smoking, diet, exercise)
-Co-morbidities (control BP, glycaemic control)
-Aspirin and clopidegrol for 1 year
-B blockers to slow heart rate
Statins
ACE inhibitors

55
Q

When are ACE inhibitors always given after a STEMI?

A

Left ventricular dysfunction

56
Q

What inpatient investigations are carried out following a STEMI?

A

-ECHO

57
Q

What are the most important determinants of MI survival?

A
  • Age

- LV ejection fraction

58
Q

What is the survival of patients resuscitated following SCD?

A

~2%

59
Q

What is the primary causes of SCD in those resuscitated?

A

80% VT or VF

60
Q

What causes ventricular arrhythmia in SCD?

A

The atherthrombotic event causes acute myocardial ischaemia and subsequent sufficient electrical distubance

61
Q

What is the only effective treatment for VF?

A

Defibrillation

62
Q

What does VF rapidly deteriorate into?

A

Asystole

63
Q

When does the best chance of success in resuscitation occur?

A

In the first 3-4 minutes

64
Q

What are the 2 main groups of immediately life threatening complications of AMI?

A
  • Mechanical complications

- Ventricular arrhythmic complications

65
Q

What is a later complication of AMI?

A

LV thrombus

66
Q

What are the most dramatic complications of MI?

A

Mechanical complications

67
Q

What are the 3 main mechanical complications of MI?

A
  • Free wall rupture
  • Papillary muscle rupture
  • Rupture of IVS
68
Q

Where does free wall rupture occur?

A

At the edge of the infarcted area

69
Q

What does free wall rupture lead to?

A
  • Haemopericardium

- Acute tamponade

70
Q

What can prevent EMD death falling free wall rupture?

A

False aneurysm or adhesions containing pericardial infusion

71
Q

Who is free wall rupture most common in?

A
  • Elderly
  • Females
  • HBP
  • Anterior MI
72
Q

What should be carried out urgently following free wall rupture?

A
  • ECHO
  • Pericardiocentesis
  • Drainage with pigtail catheter
73
Q

Who is septal wall rupture more common in?

A
  • Elderly
  • Females
  • HBP
  • Those not thrombolysed
74
Q

What type of septal wall rupture is anterior MI associated with?

A

Apical VSD

75
Q

What type of septal wall rupture is inferior MI associated with?

A

Basal VSD

76
Q

What type of papillary muscle rupture is inferior MI associated with?

A

Posterior and medial muscle

77
Q

What type of papillary muscle rupture is associated with anterior/lateral MI?

A

Anterior/lateral muscle

78
Q

When do papillary muscle rupture and VSD usually occur?

A

Within the first week following an MI

79
Q

What are the symptoms of papillary muscle rupture and VSD?

A
  • Sudden sever breathlessness
  • Autonomic activation including sweating, nausea and vomiting
  • Chest pain
80
Q

What are the signs of papillary muscle rupture and VSD?

A
  • Shock
  • Tachycardia
  • Pulmonary oedema
  • New harsh systolic murmur
  • Right parasternal heave
  • Palpable thrill
  • Elevated JVP
81
Q

How is papillary muscle rupture and VSD differentiated?

A
  • MV rupture causes more SOB and oedema
  • JVP usually more elevated with VSD
  • Inferior MI associated with MR
  • Anterior MI associated with VSD
  • ECHO used
82
Q

What might be seen on ECHO when investigating mechanical complications of MI?

A
  • Prolapsing mitral leaflet +/- chunk of muscle
  • Broad MR jet into normal size LA
  • VSD easily missed
  • RV size, function and pressure is a strong predicator of outcome with VSD
83
Q

Other than ECHO what other investigation would be performed when investigating the mechanical complications of MI?

A

-Cath lab

84
Q

Why is a right heart cath performed?

A
  • Step up in O2 sats with VSD
  • Confirms Dx and quantifies shunt
  • Large v waves on wedge with acute MR
85
Q

Why is a left cath performed?

A
  • Establish coronary anatomy

- Better localisation of pathology

86
Q

How should papillary muscle rupture and VSD be monitored?

A
  • IV nitrates if SBP>90mmHg
  • Inotropes if SBP<90mmHg
  • IABP
  • Call cardiac surgeons
87
Q

What surgery can be performed for papillary muscle rupture or VSD?

A
  • Mitral valves are usually replace rather than repaired
  • VSD repair with pericardial or synthetic patch
  • Coronary artery bypass
88
Q

Ventricular tachycardia

A

Broad complex, regular generally rapid tachycardia

-Initiated by ventricular premature beat, sustained by re-entry loop

89
Q

When does VT occur in relation to MI?

A

Any time following MI

90
Q

What can drive VT?

A

-Ischaemic and/or myocardial damage

91
Q

What is required if VT is sustained?

A
  • Urgent cardioversion
  • Electrically
  • Amiodarone or pacing
92
Q

What is the treatment for VT?

A

Medical therapy +/- ICD with anti-tachycardia pacing

93
Q

Ventricular fibrillation

A
  • Irregular ineffectual ventricular fibrillating activity

- Multiple wavelets of electrical activity

94
Q

Where are LV thrombus typically seen?

A

Apical/anteri-apical MI resulting in significant LV dysfunction

95
Q

When are LV thrombus seen in relation to MI?

A

After 48 hours

96
Q

How are LV thrombi treated?

A

Anticoagulation for 6 months with warfarin and repeated ECHOs

Systems: Cardiovascualar AB (42 decks)

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