- ACUTE CORONARY SYNDROMES - Flashcards

1
Q

Define Coronary Artery Disease (CAD)

A

An impedance or blockage of on or more arteries that supply blood to the heart, usually due to atherosclerosis

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2
Q

Outline the pathophysiology of CAD

A
  1. Endothelial dysfunction results in increased permeability, allowing excess LDL to accumulate in the intima, a chemical reaction occurs in the intima making them oxidised LDL
  2. Stimulation of the endothelial cells from reaction results in diffusion of lipids and inflammatory cells (monocytes and T lymphocytes) into endothelial cells and subendothelial spaces
  3. Monocytes and macrophages produce inflammatory mediators
  4. Macrophages ingest O-LDLs and become fat lade and frothy; these are called foam cells
  5. Foam cells form fatty streaks and promote the migration of smooth muscle cells from the tunica media to the tunica intima and this causes smooth muscle cell proliferation
  6. Increased SMC proliferation results in increased synthesis of collagen, which hardens plaque and forms a fibrous cap over lipid core, protruding into lumen
  7. Foam cells die and release lipid contents resulting in the formation of plaque
  8. With increased turbulance around protruding plaque, from HTN or increased cardiac workload, the plaque may rupture, releasing its contents.
  9. The clotting process is initiated to contain lipid contents
  10. Thrombus is formed and platelets adhere to the thrombus
  11. Thrombus then inhibits blood flow/ O2 supply to the heart
  12. ishccaemia/infarct
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3
Q

Discuss the pharmacological management of patients with chest pain

A
  • Aspirin (antiplatelet to reduce platelet aggregation and thrombus formation)
  • GTN (vascular smooth muscle relaxant - reduces preload and afterload and thus reduces O2 demmand)
  • Morphine ( reduces SNS stimulation resulting in a decrease in catecholamine realease and thus reduces O2 demmand. Also works as a vasodilator)
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4
Q

Discuss the pathophysiology of a STEMI

A

ACS pathophysiology +:

  • thrombus fully occludes the vessel and involves the full thickness of the ventricular wall
  • results in an imbalance between O2 supply and demmand to the myocardial cells
  • ischaemia
  • cell injury/death
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5
Q

Discuss the management of a STEMI

A
  • Code STEMI
  • Drugs (Aspirin, anti-platelet, heparin)
  • PCI (percutaneous coronary intervention - cath lab) <60 mins
  • Throbolysis should be considered if PCI unavailable
  • CABGS
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6
Q

Describe how to differentiate between cardiac pain and non-cardiac pain

A
  • nature
  • location
  • radiation
  • precipitating/relieving factors
  • Assoc clinical manifestations
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7
Q

Describe conditions that cause ischaemic cardiac chest pain and non-ischaemic cardiac chest pain

A

Ischaemic cardiac chest pain (angina)

  • CAD (atherosclerosis)
  • blood clots
  • coronary artery spasm
  • trauma
  • MI

Non-Ischaemic cardiac chest pain

  • pericarditis
  • myocarditis
  • dissecting aortic aneurysm
  • atypical ballooning syndrome (takotsudo cardimyopathy)
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8
Q

Outline patient selection criteria for reperfusion therapy

A

Is the PCI delay time <90mins?

  • door to needle (D2N)
  • door to balloon (D2B)
  • PCI delay = D2B - D2N
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9
Q

List absolute contraindications to thrombolytic therapy

A
  • ischaemic CVA within 3 months
  • Intracranial CA
  • Aortic dissection
  • active bleeding
  • head trauma < 3 months ago
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10
Q

Outline four (4) clinical signs which may indicate that reperfusion has been successful

A

. - ST segment recovery

  • QRS vector changes
  • re-perfusion arrhythmias
  • T wave configuration changes
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11
Q

Briefly outline nursing priorities for a patient undergoing reperfusion therapy

A
  • swift assessment for reperfusion contraindications
  • pt education (risk of bleeding, having to stay still)
  • swift preparation of pt (large bore IVs, ECG, pedal pulses, checklist)
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12
Q

List the complications that may occur post AMI

A
  1. Ischaemic complications (reperfusion failure, angina, infarction, infarction extension)
  2. Mechanical complications (cardiogenic shock, MV dysfunction, cardiac rupture)
  3. Throbosis and embolic complications (CNS or peripheral embolisation)
  4. Chronic complications (pericarditis, depression)
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13
Q

State the clinical indications for recording a right and posterior ECG

A

Right sided ECG:
- in the case of an inferior AMI (STE in II,III,aVF)

Posterior ECG
- STD in V1-3

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14
Q

Specify where you will place the V leads to record a right and posterior ECG

A

Right:
V1-6 are placed in a mirror image fashion from standard precordial leads

Posterior:
V4-6 are moved to the posterior of the L chest in lead V7-9 positions

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15
Q

Describe the clinical implications of a pathological Q wave

A

Pathological Q waves may indicate:

  • MI
  • Cardiomyopathies
  • Rotation of the heart
  • Incorrect lead placement
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16
Q

Define unstable angina

A
  • occuring at random and at rest
  • no particular pattern
  • lasts longer than 20 mins
17
Q

Describe the desired action of Aspirin in the acute coronary syndrome (ACS) patient

A
  • antiplatelet to reduce platelet aggregation and thrombus formation
18
Q

List anti-platelet therapies, other than Aspirin, that are available in your ED and describe their mode of action

A
  • clopidogrel
19
Q

Discuss the action of nitrates in the ACS patient

A
  • vascular smooth muscle relaxant - reduces preload and afterload and thus reduces O2 demmand
20
Q

Explain the action of beta-blockers in the ACS patient

A
  • Inhibit chronic activation of neuro-hormonal system
  • Positive ionotropic and chronotropic responses
  • Allow for renal and systemic vasodilation
21
Q

Identify the thrombolytic agents are available in your ED and explain their specific mode of action for each

A
  • Alterplase
  • Reteplase
  • Tenecteplase
22
Q

Outline the nursing management of the patient receiving thrombolysis

A
  • Identify and contraindications
  • Educate pt on risk of bleeding
  • Set up of infusion
  • Assess vital signs frequently
  • continuous cardiac monitoring
  • evaluate response to therapy
  • bed rest for 6 hrs
  • monitor body fluid and assess for any signs of haemorrhage
  • monitor for early signs of re-occlusion
23
Q

Identify the modifiable for CAD

A
  • cigarette smoking
  • obesity
  • hypertension
  • physical inactivity
  • kidney disease
  • diabetes mellitus
  • alcohol consumption
  • stress
  • elevated LDL
  • reduced HDL
24
Q

Identify the non-modifiable for CAD

A
  • males >45 years
  • females >55 years
  • PHx of CAD
25
Q

Discuss the pathophysiology of an NSTEMI

A

ACS pathophysiology +:

- formation of a non - occlusive thrombus which limits myocardial perfusion

26
Q

Discuss the diagnostic criteria of a STEMI

A
  • ACS with ECG changes
  • ST elevation >2mm in 2 or more precordial chest leads
  • ST elevation >1mm in 2 or more limb leads
  • new LBBB pattern
27
Q

Discuss the diagnostic criteria of an NSTEMI

A
  • Typical/atypical CP, age risk factors, ECG changes
  • abnormal, dynamic ST segment deviation >0.5mm or new T wave inversion >2mm
  • ECG may be normal, changes in only 50% of cases
  • ACS without ECG changes but with a rise in troponin
28
Q

Discuss the management of an NSTEMI

A
  • Aspirin
  • Risk stratification (high, intermediate, low)
    High - antiplatelet, PCI and re-vascularisation
    Intermediate - Observe with frequent ECGs, repeat troponin, provocative testing to promote re-classification
    Low - assessed and d/c on increase blood thinners and early OP cardiologist r/v
29
Q

List relative contraindications to thrombolytic therapy

A
  • HTN >180/110
  • ischaemic CVA > 3 months ago
  • dementia
  • intracranial disease
  • traumatic or prolonged CPR
  • major symptoms in the past 3 weeks
  • internal bleeding past 2-4 weeks
  • non-compressible vascular punctures
  • pregnancy
  • current anticoagulation therapy