ACS Flashcards

1
Q

What is the pathophysiology of ACS?

A

Artheromstous plaque formation in coronary vasculature, exposing fibrin, collagen, cholesterol and cellular debris
This creates stimulation for: platelet adhesion, aggregation, thrombus formation and localised vasoconstriction

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2
Q

ACS is a …

A

Critical stage of IHD with differing degrees of occlusion and embolisation

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3
Q

What is the pathophysiology for a stable angina?

A

Stable intact lesion

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4
Q

What is the pathophysiology of unstable angina?

A

Breached endothelium with or without superimposed fibrin clot and coronary spasm

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5
Q

What is the pathophysiology of an MI?

A

Plaque rupture with superimposed fibrin clot leading to total coronary occlusion and coronary spasm

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6
Q

How do you diagnose ACS?

A

Pt history
Typical symptoms
ECG changes
Biochemical markers

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7
Q

What is the rational for the assessment of ACS?

A
Diagnostic
Therapeutic
Humanistic concern
Improve and maintain pt nurse relationship
Accountability
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8
Q

What are the possible differential diagnosis for a of presenting with ACS?

A
Angina pectoris
MI
Pericarditis
Dissecting aortic aneurysm 
Tracheobronchitis
Pleural pain
Reflux oesphagitis
Chest wall pain
Anxiety
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9
Q

What is the PQRST assessment of chest pain?

A
Precipitating factors
Qualitative factors
Region and radiation
Severity and associated symptoms
Timing
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10
Q

What is included in precipitating factors for Chest pain assessment?

A

What factors precipitated discomfort?

What was happening at symptom onset?

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11
Q

What is included in qualitative factors in chest pain assessment?

A

Describe pain
What does pain feel like in own words
How did or feel at time of pain?

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12
Q

What is included in region and radiation for chest pain assessment?

A

Where and how far pain spreads

Pain normally in left arm, inner aspect of arm sometimes as far as fingers, jaw (not to ear), neck, back, epigastrium

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13
Q

What is included in severity and associated symptoms for chest pain assessment?

A

How bad is the pain?
0-10
Aware of any other pain?

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14
Q

What is included in timing for the chest pain assessment?

A

How long did it last?

What makes the pain better?

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15
Q

What are the or groups with atypical presentations of ACS?

A

Women
Elderly
Diabetes
Ethnic minority

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16
Q

What are the risk factors for ACS?

A
Smoking
Hypercholestraemia
Diet
Sedentary lifestyle
Alcohol consumption
Hypertension
Obesity
Socioeconomic deprivation 
Diabetes
17
Q

What are the symptoms of ACS?

A
Chest pain
Hypotension
Autonomic nervous system activation
Pallor
Sweating
Rhythm disturbances
18
Q

What does ST depression mean?

A

Ischaemia, left ventricular hypertrophy,

Digoxin toxicity

19
Q

What does ST elevation mean?

A

Acute MI

20
Q

What does T wave flattening mean?

A

Ischaemia and hypokalaemia

21
Q

What are the STEMI ECG changes?

A
Total coronary occlusion
Ongoing chest pain
Persistent ST elevation
New LBBB
Raised biochemical markers
22
Q

What are the non STEMI ECG changes?

A

Acute ishaemic event
Chest pain
Various ECG changes: persistent ST depression and/or T wave inversion, flattened T waves, normal ECG
Raised biochemical markers

23
Q

What are the biochemical markers associated with ACS and how long are they present?

A

CK creatin kinase: released after irreversible clear injury from hypoxia, takes 4-6 hrs to rise and 24hrs to peak
Troponin: released after myocardial damage, 3-4 hrs to detect and elevated 1-2 weeks

24
Q

What is the treatment for an MI?

A
Immediate treatment
ECG
Aspirin 300 mg chewed
Clopidogrel
Pain relief
25
Q

What are the key priorities NICE guidelines (2010) for ACS?

A

12 lead ECG asap
Recording and sending ECG should not delay transfer to hospital
Don’t routinely administer O2 (monitor SATs)
Don’t assess symptoms of an ACS differently in ethnic groups

26
Q

What is the treatment for angina?

A

Drugs that reduce cardiac workload: beta blockers, nitrates, calcium channel blockers
Drugs that reduce the risk of infarction: anti platelet drugs
Drugs that reduce cholesterol: statins

27
Q

What is the treatment for MI?

A

Primary angioplasty reduces death, stroke and non fatal infarction
CABG of diffuse disease
PTCA
PCI = reperfusion and stroke reduction benefits after 3 hrs
Thrombolysis where no PCI available

28
Q

What are the benefits of primary angioplasty for ACS pts?

A
More effective restoration of patency
Improved LV function
Reduction in re-occlusion
Reduced stroke risk
Improved survival
Reduction in hospital stay
29
Q

What is the continuing care of a pt with an MI?

A

Monitor for arrhythimas
Pain management
Secondary prevention/rehab (lifestyle, cardiac rehab, drug therapy, cardiologist review)

30
Q

What is cardiac rehab?

A

Tailored to individual needs
Culturally sensitive
Includes: health education, stress management and exercises

31
Q

What is the drug therapy for pts post MI?

A
ACE inhibitors
Aspirin indefinitely
Clopidogrel
Beta blockers 
Statins
32
Q

What is the definition of ACS?

A

A combination of clinical signs and symptoms resulting from myocardial ischaemia
Includes: unstable angina, STEMI and non STEMI