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Flashcards in Acute MI Deck (71)
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1
Q

Heart risk examples?

A

Smoking and stress Alcohol - Hypertension Drug abuse- High cholesterol Age - Obesity Gender - Family history

2
Q

Process of Atherogenesis?

A

Normal | } Clinically silent Fatty streak | Atheromatous plaque | } Angina and claudication Atherosclerotic plaque

3
Q

Describe chronic stable angina?

A

Predictable Fixed stenosis Demand led ischaemia Safe

4
Q

How to treat chronic stable angina?

A

Stop Sit Spray (GTN)

5
Q

Ways of describing chest pain?

A

Heavy feeling Weight on chest Pressure Tightness

6
Q

In depth description of the atherosclerotic process?

A

T-he development of atheroma begins with the deposition of a fatty streak within the wall of a vessel. -Over time, this initial lesion develops firstly into an atheromatous plaque and subsequently to an area of atherosclerosis. These two stages are often completely asymptomatic, although the lesion may occlude the vessel lumen sufficiently to give rise to symptoms such as angina or claudication during exercise or to transient ischaemic attacks. - The atherosclerotic plaque, particularly when it is mature and calcified, is a relatively inflexible structure and is prone to fissuring and rupture. These events in turn may trigger the development of a thrombus which can cause acute vascular stenosis, leading to local ischaemia and possibly to infarction. Depending on the vessel involved, this can become manifest as a myocardial infarction, stroke, critical leg ischaemia, or even cardiovascular death.

7
Q

What is a STEMI?

A

ST elevation MI

8
Q

What is an NSTEMI?

A

Non ST elevation MI

9
Q

What is an NSTEMI?

A

Non ST elevation MI

10
Q

Detailed Process of atherothrombosis?

A
  • The arterial endothelium is damaged initially by uneven or high ‘shear forces’ in the blood (related to abnormal pressure/flow relationships and enhanced by hypertension, hypercholesterolaemia, smoking, diabetes, inflammation and immune processes). - Lipids accumulate within the intima of the artery at a site of damage. - Over the years, fatty streaks grow towards the media of the artery and may become fibrous because of the production of collagen. Plaques are formed. - If the plaque grows into the arterial lumen, it causes further uneven blood flow and increased shear stress. This increases the build-up of plaque and stenosis of the artery. - The first symptom of arterial stenosis may be pain or cramps at times when the blood flow cannot keep up with the body’s demand for oxygen. Typically, these symptoms develop gradually as the plaque slowly narrows the artery. - At some point, plaques with a high lipid content, which are soft and unstable, may rupture and cause an acute blockage. - During plaque rupture, the lipid core and underlying endothelium is exposed to platelets in the blood. These adhere to the injured surface and release mediators, such as adenosine diphosphate (ADP) and thromboxane A2 (TXA2), that trigger platelet aggregation. - Circulating platelets aggregate at the site of injury forming a platelet-rich thrombus through further platelet activation and recruitment. This process is known as atherothrombosis.
11
Q

Acute coronary syndromes?

A

Unstable angina MI sudden Cardiac death

12
Q

What is an acute coronary syndrome?

A

Acute presentation of CAD

13
Q

Describe acute coronary syndrome?

A

Dynamic stenosis - subtotal or complete occlusion Supply led ischaemia Unpredictable Dangerous

14
Q

Factors that affect plaque rupture (fissure)

A

Lipid content of plaque (higher = more likely to burst) Thickness of fibrous cap Sudden changes in intraluminal pressure or tone Bending/twisting of an artery in each heart contraction Plaque shape Mechanical Injury

15
Q

Process of a platelet cascade?

A

Initiation - spontaneous plaque rupture Adhesion- Platelet recruitment and adhesion at the sit of injury - forming monolayer Activation- adhesion leads to this Release of activators- ADP etc is released through degranulation Surface receptors- ADP binds to receptors Amplification of platelet activation - this accelerates and leads to platelet aggregration Inflamattory cascade triggered-

16
Q

Description of an acute MI?

A

Severe crushing central chest pain Radiating to jaw and arms especially left Similar to angina but more sever and prolonged- not relieved by GTN spray Sweating, nausea and vomiting

17
Q

Angina attack vs. Acute MI details

A

Angina MI - 10 mins -30 mins or longer - Onset=exertion -At rest - Severity usual pain -More severe - GTN= Relief -No effect - No associated symptoms -Sweating, nausea & vomiting

18
Q

ECG changes in an acute STEMI?

A

ST elevation T wave inversion Q wave formation

19
Q

Detailed description of an ECG in STEMI?

A

-ST elevation 1mm< in 2 adjacent limb leads - >2mm ST elevation in at least 2 contiguous precordial leads -New onset bundle branch block

20
Q

What does an old MI look like on an ECG?

A

Q waves +- inverted T waves

21
Q

What a change in the ECG at leads 2,3 and AVF say about its anatomical position?

A

Inferior

22
Q

What leads are affected in an anterior MI?

A

V1-V6

23
Q

What leads are affected in anteroseptal MI?

A

V1-V4

24
Q

What a change in leads 1, AVL and V1-V6 say about the anatomical position of the MI?

A

Anterolateral

25
Q

What is troponin?

A

Protein Marker Highly specific for cardiac muscle damage Can detect tiny amounts of cardiac necrosis

26
Q

Mode of action of aspirin and thienopyridines

A

ASA inhibits COX, preventing the production of prostaglandin and thromboxane A2 (TxA2) from arachidonic acid. TxA2 aids the expression of the GP IIb/IIIa binding site on the platelet, allowing fibrinogen to bind. Clopidogrel is a potent inhibitor of ADP-induced platelet aggregation, irreversibly inhibiting the binding of ADP to its platelet membrane receptors. ADP binding is necessary for activation of the GP IIb/IIIa receptor, which is the binding site for fibrinogen. Clopidogrel thus ultimately inhibits the activation of the GP IIb/IIIa receptor and its binding to fibrinogen. Due to the different mode of action of aspirin and clopidogrel, the initial interest was to determine which antiplatelet was most effective at reducing vascular events

27
Q

Indications for reperfusion therapy?

A

Chest pain suggestive of acute MI ECG changes No contraindications

28
Q

Risks of thrombolytic therapy?

A

-Failure to perfuse - Haemorrhage - Hypersensitivity +

29
Q

Early treatment of STEMI?

A

Analgesia - diamorphine (IV) Anti-emetic Aspirin GTN if BP is above 90mmHg Oxygen if hypoxic Primary angioplasty Thrombolysis if angioplasty not available within 2 hours

30
Q

Complications of acute MI?

A

Death Arrhythmic complications Structural complications Functional complications

31
Q

Examples of structural complications from an MI?

A

Cardiac rupture Ventricular septal defect Mitral valve regurgitation Left ventricular aneurysm formation Mural thrombus Inflammation Acute pericarditis

32
Q

Functional complications of an MI?

A

Acute ventricular failure - left, right or both Chronic cardiac failure Cardiogenic shock

33
Q

Killip classification for heart failure?

A

1- no signs of heart failure (6%) 2- Crepitations <50% of lung fields (18%) 3- Crepitations >50% of lung fields (38%) 4- Cardiogenic shock (81% of CCF)

34
Q

Routine observations for heart failure?

A

Cardiac monitor - rhythm How does patient feel Pulse and BP Hear sounds especially added sounds Murmurs Pulmonary crepitations Fluid balance especially fluid output

35
Q

The most important thing to remember about in an acute NSTEMIs?

A

The ECG may be normal

36
Q

What does troponin C bind?

A

Calcium (for both cardiac and skeletal muscles)

37
Q

What does troponin 1 do?

A

In the absence of Ca++ it binds to actin which inhibits actin-myosin ATPase induced contraction - cardiac specific isoforms Short= Inhibits actin-myosin interactions

38
Q

What is Troponin 1 specific to?

A

Cardiac muscle

39
Q

What does Troponin T do?

A

Links troponin complex to tropomyosin which facilitates contraction - cardaic specific isoform Short= Binds with tropomyosin and facilitates contractions

40
Q

Where are troponin T and 1 located?

A

Integral components of the myofibrillar contractile apparatus of the heart

41
Q

Which are the preferred biomarkers for heart attacks?

A

Troponin T & 1 (TnT & Tn1)

42
Q

Why are troponins the gold standard biomarkers?

A

Nearly absolute myocardial specificity-highly sensitive They reflect the microscopic zone of myocyte necrosis Suggestion that any amount of Myocardial ischaemia should be labelled as MI

43
Q

What are we measuring with troponin?

A

Embolization Microvascular circulation Myonecrosis `

44
Q

What is serial Tn testing used for?

A

To discriminate between acute and chronic events

45
Q

Diagram of adhesion, activation and aggreggation?

A
46
Q

What is the final common pathway leading to platelet aggregation and thrombus formation?

A

GP-IIb-IIIa

47
Q

What happens in GP IIb-IIIa?

A

The expression of GP IIb-IIIa and the cross-linking of platelet receptors GP IIb-IIIa by fibrinogen molecules

48
Q

What is a GRACE calculator?

A

Risk calculator for death or MI from admission to hospital to 6 months after discharge

49
Q

How are stents inserted?

A

Catheter inserted

Balloon inflated

Stent remains

50
Q

Troponin-itis?

A

When clinicains diagnose patients with acute MI only on the fact that they have elevated troponin

51
Q

What other conditions are troponin elevated in?

A

CCF

Hypertensive crisis

Renal failure

Pulmonary embolism

Sepsis

Stronk (TIA)

Peri/myo carditis

Post arrhythmia

52
Q

Detailed diagnostic process for an MI?

A
  • Detect rise/fall of cardiac biomarker values (preferably cardiac Tn with atleast one value above the 99th percentile upper refernce limit [URL])
  • One of these other criteria
  • Symptoms of ischaemia
  • New or presumed new signif ST segment- T wave changes or new left bundle branch block. Development of pathological Q waves in the ECG
  • Imgaing evidence of new loss of viable myocardium or new regional wallmotion abnormality
  • ID of an intracoronary thrombus by angiography or autopsy
53
Q

Diagnosis of an AMI simple explanation?

A

Troponin measurement is central and tested before symptoms

HOWEVER

You need atleast 1 of 4 additional criteria to diagnose an AMI

54
Q
A
55
Q

Definition of an MI classification 1?

A

Spontaenous MI related to ischaemia due to primary coronary event such as plaque erosion and/or rupture, fissuring or dissection

56
Q

Definition of an MI classification 2?

A

MI secondary to ischaemia due to an imbalance of O2 supply and demand, as from coronary spasm or embolism, anaemia, arrhythmias, hypertension or hypotension

57
Q

Definition of an MI classification 3?

A

Sudden unexpected cardiac death. including cardiac arrest often with symptoms suggesting ischaemia with new ST- segment elevation, new left bundle branch block: or pathollogic/ angiographic evidence of fresh coronary thrombus

58
Q

What is a type 2 myocardial infarction?

A

Secondary to ischaemic imbalance

Increased myocardial oxygen demand or reduced myocardial oxygen

59
Q

Example’s of conditions causing increased myocardial oxygen demand are?

A

Sustained tachycardia

Significant hypertension

Mared left ventricular hypertrophy

Hypertrophic cardiacmyopathy

Valvular disease

60
Q

Conditions causing reduced myocardial blood flow include?

A

Anaemia

Hypoxia (resp failure)

Bradychardia

Hypotension

Vasospasm

Coronary embolism

61
Q

Causes of type 2 MI?

A

It is an MI due to ischaemic imbalance

Causes:

Increased myocardial O2 demand

Decreased myocardial 02/Blood flow

62
Q

Typical features of a type 1 MI?

A

Sudden symptoms

Major ECG changes

No other obvious causes

Higher trop with rise then fall

Severe CAD on angiography

63
Q

Typical features of a type 2 MI?

A

Less chest pain

Minor ECG changes

Tach/ BP low / illness

Smaller more static trop

Mild moderate coronary disease

64
Q

What is non-ischaemic myocardial injury with necrosis?

A

Not technically a Type II MI but often labelled as such due to difficulties with classification
Usually occurs in complex patients with significant medical or surgical issues
Seriously unwell patients or chronic disease patients but without evidence of significant coronary artery disease absence of ischemic symptoms or ECG changes
Within this group it becomes much harder when patients develop some ischaemic features or minor ECG changes where the diagnosis might revert to Type I or II MI

65
Q

Examples of cardiac injury not related to myocardial ischaemia?

A

Cardiac contusion

Ablation

Pacing

AICD shocks

Myocarditis

Cardiotoxic chemotherapy

66
Q

Conditions associated with non-ischaemic myoardial injury with necrosis?

A

Cardiac inury not related to myocardial ischaemia

Multifactorial or indetreminate myocardial injury

67
Q

Examples of multufactorial or indeterminate myocardial injury?

A

Severe sepsis or renal failure

Pulmonary embolus, pulmonary hypertension, cor pulmonale

Chronic severe heart failure, chronic renal failure

Seveer acute neurological diseases- stronk

Excercise, burns

Stress cardiomyopathy (takotsubo)

68
Q

Seconday prevention methods?

A

Healthy lifestyle

Smoking cessation

Good control of BP, cholesterol and diabetes

69
Q

4 phases of rehabilitation?

A

In- patient

Early post-discharge period

Structured excercise programme - hospital based

Long term maintenance of physical activity and lifestyle change (community based)

70
Q

Targets for secondary cardiac MI prevention?

A

Avoid smoking

Healthy diet

Regular aerobic exercise

Optimal drug therapy

Cholesterol ,4.0 mmol/l

BP <140/85 mmHg

71
Q

Heart attack tablets?

A
  • Aspirin/clopidogrel
  • Ateno