Diagnosis and management of acute coronary syndromes - STEMI Flashcards

(42 cards)

1
Q

What is the pathology of a ST-elevation myocardial infarction

A

Plaque rupture leads to more complete, or complete thrombotic occlusion of coronary lumen and infarction of distal myocardium

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2
Q

What can be seen on an ECG of STEMI

A

ST elevation

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3
Q

What further problems arise due to coronary occlusion

A

Necrosis of myocardial tissue

Left ventricular damage

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4
Q

How can myocardial tissue be salvaged in a coronary occlusion and what are the treatment options

A

“open” infarct related artery

By Fibrinolysis or Primary PCI

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5
Q

What is the benefits of primary PCI over fibrinolytic therapy

A

Has a greater reduced risk of cardiac mortality, recurrent MI; and haemorrhagic stroke

PCI is most effective if delivered within 120 to 150 mins of the patient’s call for help

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6
Q

When would fibrinolytic therapy be the treatment of choice and What is the times of fibrinolytic therapy from the call and entering the hospital

A

when PCI cannot be performed

Aim to initiate within
(‘call-to-needle’) 90 mins of patient calling for help

(‘door-to-needle’) within 30 mins of hospital arrival

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7
Q

When is it best to perform PCI

A

If can be delivered in less than 90minutes from call for help and has more than 3 hours symptom onset

Cardiogenic shock or heart failure present

High bleeding risk

Diagnosis uncertain e.g coronary dissection

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8
Q

What is the general measures of secondary preventions put in place to reduces the risk of STEMI

A

General measures:
stop smoking, diet, exercise, control BP and glycemic

Statins
Angiotensin converting enzyme inhibitors - rampipril
- if left ventricular dysfunction

also:
Beta blocker

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9
Q

What is the dual medication therapy that must be taken for one year after STEMI as a prevention therapy

A

Aspirin and clopidogrel (for one year only)

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10
Q

What possible myocardial disfunction does an ECHO show

A

Size of wall motion abnormality

overall contractility

presence and degree of mitral regurgitation

presence of mural thrombus

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11
Q

LV ejection is the most important factor to investigate in MI survival, what does it show?

A

how well your left ventricle (or right ventricle) pumps blood with each heart beat - show if any LV dysfunction

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12
Q

How can ACS result in sudden cardiac death

A

As an ACS, the atherothrombotic event causes acute myocardial ischaemia and subsequent sufficient electrical disturbance to cause ventricular arrhythmia
ventricular Fibrillation tends to rapidly deteriorate into asystole - heart ceases to beat

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13
Q

What can be seen on an ECG of sudden cardiac death

A

Irregular, ineffectual ventricular fibrillating activity

Multiple wavelets of electrical activity

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14
Q

What is the appropriate plane when ventricular arrest happens (sudden cardiac death)

A

Resuscitation: Defibrillation with the best chance for success probably occurring in the first 3–4 minutes

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15
Q

What is the two main groups of immediately life threatening complications of acute MI,

A

Mechanical complications

Ventricular arrhythmic complications

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16
Q

What is a later complication of acute MI less threatening but still needs treatment

A

LV thrombus

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17
Q

What is the three main mechanical complications

A

Free Wall Rupture
Papillary Muscle Rupture
Ventral Septal defect

18
Q

Where is free wall rupture most likely to occur and what is the outcome

A

Occurs at the edge of the infarcted area

haemopericardium - blood effuses into pericardium resulting in acute tamponade which compreses the heart due to fluid compression in the pericardium

19
Q

What patients are more common to experience a mechanical complication after a AMI

A
Elderly, 
females, 
Patients with HBP 
Or patient who experienced an anterior MI
Patients who have not been thrombolysed
20
Q

What is the treatment if possible for a free wall rupture

A

urgent echo,

pericardiocentesis and drainage with pigtail catheter.

21
Q

In what patients is it more likely for septal wall rupture (VSD) to occur

A

Patients with multi vessel CAD

22
Q

When in papillary muscle rupture and Ventral septal defect most likely to occur

A

Generally within the first week of MI.

23
Q

What is the symptoms of papillary muscle rupture and Ventral septal defect

A

Sudden severe breathlessness
Autonomic activation eg sweating, nausea & vomiting
Chest pain

24
Q

What is the signs of papillary muscle rupture and Ventral septal defect

A
Shock, tachycardia, 
pulmonary oedema
New harsh systolic murmur
Right parasternal heave
Palpable thrill
elevated JVP.
25
What can occur as a result of papillary muscle rupture and worsen symptoms
Mitral valve regurgitation
26
What mechanical complication has the greatest elevation in JVP
Ventral Septal defect
27
What mechanical complication is most likely to develop an Inferior MI anterior MI
Papillary muscle rupture Ventral septal defect
28
What does an echo show in investigation mechanical complication of an AMI and what can easily be missed
Prolapsing mitral leaflets Missing chunks of muscle a VSD can be easily missed
29
How does right heart catheterization confirm the diagnosis of mechanical complication
VSD - shown by a Step up in O2 sats | Acute mitral regurgitation - Large v waves on wedge
30
What is the purpose of catheterization
Establish coronary anatomy | Better localisation of pathology
31
What is the temporary medical management of papillary muscle rupture and VSD dependant on blood pressure
I.V. Nitrates if Systolic BP > 90mmhg or Inotropes if Systolic BP < 90mmhg
32
How does IABP (balloon pump) aid in the treatment of papillary muscle rupture and VSD
Reduce afterload, therefore increasing Diastolic BP
33
What is the Non pharmaceutical treatments for papillary muscle rupture and VSD
surgery - coronary bypass if needed - Miral valve replacemrnt - VD repair with pericardial or synthetic patch Balloon pump
34
What is examples of Ventricular arrhythmic complications
Ventricular tachycardia | Ventricular Fibrillation
35
What is the ECG characteristics that help define VTs:
Rapid, wide, and regular QRS complexes Rate of 120 BPM or greater The T-waves are large with deflections opposite the QRS complexes P-waves are usually not visible, therefore the PR interval is not measurable
36
What is the medical treatment for VT
Cardioversion - electric shocks to your heart through electrodes placed on your chest amiodarone -antiarrhythmic medication used to treat and prevent a number of types of irregular heartbeats
37
What can be seen in VF
P-waves and QRS complexes are not present Heart rhythm is highly irregular The heart rate is not defined (without QRS complexes) multiple wavelets
38
What is the only possible medical treatment for VF
Defibrillation -the stopping of fibrillation of the heart by administering a controlled electric shock, to allow restoration of the normal rhythm
39
What is the general outcome of VF
asytole - difficult to restore cardiac output
40
What maintains VF
the multiple wavelets
41
What is the result of a LV thrombus
significant LV dysfunction
42
What is the treatment for LV thrombus
Anticoagulation for 6/12 with warfarin and repeat echo