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Cardiovascular system SA > Diagnosis and management of acute coronary syndromes - STEMI > Flashcards

Diagnosis and management of acute coronary syndromes - STEMI Flashcards

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
Q

What can occur as a result of papillary muscle rupture and worsen symptoms

A

Mitral valve regurgitation

26
Q

What mechanical complication has the greatest elevation in JVP

A

Ventral Septal defect

27
Q

What mechanical complication is most likely to develop an
Inferior MI
anterior MI

A

Papillary muscle rupture

Ventral septal defect

28
Q

What does an echo show in investigation mechanical complication of an AMI and what can easily be missed

A

Prolapsing mitral leaflets
Missing chunks of muscle

a VSD can be easily missed

29
Q

How does right heart catheterization confirm the diagnosis of mechanical complication

A

VSD - shown by a Step up in O2 sats

Acute mitral regurgitation - Large v waves on wedge

30
Q

What is the purpose of catheterization

A

Establish coronary anatomy

Better localisation of pathology

31
Q

What is the temporary medical management of papillary muscle rupture and VSD dependant on blood pressure

A

I.V. Nitrates if Systolic BP > 90mmhg
or
Inotropes if Systolic BP < 90mmhg

32
Q

How does IABP (balloon pump) aid in the treatment of papillary muscle rupture and VSD

A

Reduce afterload, therefore increasing Diastolic BP

33
Q

What is the Non pharmaceutical treatments for papillary muscle rupture and VSD

A

surgery

  • coronary bypass if needed
  • Miral valve replacemrnt
  • VD repair with pericardial or synthetic patch

Balloon pump

34
Q

What is examples of Ventricular arrhythmic complications

A

Ventricular tachycardia

Ventricular Fibrillation

35
Q

What is the ECG characteristics that help define VTs:

A

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
Q

What is the medical treatment for VT

A

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
Q

What can be seen in VF

A

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
Q

What is the only possible medical treatment for VF

A

Defibrillation -the stopping of fibrillation of the heart by administering a controlled electric shock, to allow restoration of the normal rhythm

39
Q

What is the general outcome of VF

A

asytole - difficult to restore cardiac output

40
Q

What maintains VF

A

the multiple wavelets

41
Q

What is the result of a LV thrombus

A

significant LV dysfunction

42
Q

What is the treatment for LV thrombus

A

Anticoagulation for 6/12 with warfarin and repeat echo

Cardiovascular system SA (43 decks)

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