NURS5084 Nursing the Acutely Ill Person Week 1.1: Introduction to Nursing the Acutely Ill Person Week 1.2: Acute coronary syndromes Structure of the heart Conduction system of the heart SA and AV Node o All myocardial cells are capable of generating an impulse (automaticity) o Impulses begin in the SA node (located at top of right atrium) o SA node has fastest intrinsic rate of cardiac cells o Impulse then spreads through 3 conduction pathways to the AV node Delays cardiac impulse to allow for atrial kick that helps to fill the ventricles Controls the number of impulses reaching the ventricles Bundle Branches and Purkinje system o The electrical impulse then travels from the AV node to the left and right bundle branches o Each bundle branch ends in a network of fibres called the Purkinje system which stimulate ventricular contraction Coronary circulation Right Coronary Artery (RCA) o Usually supplies right atrium, right ventricle and inferior wall of left ventricle o Supplies SA node in 55% of people and AV node in 90% Normal coronary circulation o Left anterior descending artery: supplies the left atrium and anterior wall of the left ventricle o Left circumflex artery: supplies left atrium and lateral and posterior walls of the left ventricle
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NURS5084 Nursing the Acutely Ill Person · 2018-01-25 · o Pleuritic pain? Pain unlikely to be of cardiac origin o Pain mainly located in the middle/lower abdomen o Pain that can
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NURS5084 Nursing the Acutely Ill Person
Week 1.1: Introduction to Nursing the Acutely Ill Person
Week 1.2: Acute coronary syndromes
Structure of the heart
Conduction system of the heart
SA and AV Node
o All myocardial cells are capable of generating an impulse (automaticity)
o Impulses begin in the SA node (located at top of right atrium)
o SA node has fastest intrinsic rate of cardiac cells
o Impulse then spreads through 3 conduction
pathways to the AV node
Delays cardiac impulse to allow for atrial
kick that helps to fill the ventricles
Controls the number of impulses reaching
the ventricles
Bundle Branches and Purkinje system
o The electrical impulse then travels from the AV
node to the left and right bundle branches
o Each bundle branch ends in a network of fibres
called the Purkinje system which stimulate
ventricular contraction
Coronary circulation
Right Coronary Artery (RCA)
o Usually supplies right atrium,
right ventricle and inferior wall of
left ventricle
o Supplies SA node in 55% of
people and AV node in 90%
Normal coronary circulation
o Left anterior descending artery:
supplies the left atrium and anterior wall of the left ventricle
o Left circumflex artery: supplies left atrium and lateral and posterior walls of the left ventricle
o Supplies SA node in 45% of people and AV node in 10%
Potential intercoronary channels between arterial branches provide possibility for collateral circulation
Risk factors for Coronary Artery Disease
Unmodifiable
o Male gender
o Post-menopausal female
o Family history
o 65+ years
Modifiable
o Smoking
o Overweight/obesity (BMI, hip:waist
ratio)
o Hypertension
o Hyperlipidaemia
o Depression
o Diabetes
o Physical inactivity
Cardiac pain
Typical cardiac pain
o Central or left-sided tightness, heaviness, discomfort
o May radiate to arms (especially left), throat, back or epigastric area
o May be associated with diaphoresis, SOB, dizziness, nausea/vomiting
Atypical cardiac pain
o Seen especially in the elderly, diabetics and women
o Epigastric pain only
o Pain or heaviness in arms only
o Pain or tightness in jaw or throat only
o Associated with fatigue and SOB
o Pleuritic pain?
Pain unlikely to be of cardiac origin
o Pain mainly located in the middle/lower abdomen
o Pain that can be localised by the tip of 1 finger – especially if over the LV apex
o Pain reproduced with movement or palpation of the chest wall or arms
o Constant pain lasting many hours with a normal ECG
o Brief episodes of pain lasting only a few seconds
o Pain that radiates into lower extremities
Coronary artery disease and stable angina
CAD = when plaque builds up on the intima (inner lining) of the arterial wall, partially occluding the artery
This may result in stable angina (predictable symptoms that occur in response to predictable stimuli)
o Deep, poorly localised chest/arm discomfort (+/- SOB)
o Comes on predictably with physical exertion, emotional stress
o Relieved promptly with rest and/or sublingual nitrates
o Not a medical emergency; patients with known stable angina should seek review if pain becomes:
More severe
Occurs more frequently
Lasts >10 minutes
Comes on at rest
o May be treated with:
Angioplasty and stenting
Coronary artery grafting
Pharmacological management
Acute Coronary Syndromes (ACS)
Pathophysiology: rupture/erosion of atheromatous plaque triggers clotting mechanism (thrombus
formation) total/partial occlusion of the artery
Unstable Angina Pectoris (UAP): chest pain/discomfort but no permanent injury
o Temporary/partial occlusion local ischaemia
o Diagnosis on clinical history and ECG
o ST segment depression >0.5mm
o T-wave inversion or flattening
o Some will have normal ECG
o Normal cardiac enzymes (Troponin)
o Patients with UAP are at high risk of death
Non ST Elevation Myocardial Infarction (NSTEMI): smaller area of infarction (permanent injury) often due
to transient/partial occlusion
o Plaque rupture
o Thrombus formation and arterial occlusion for up to 1hr
o Area of cell necrosis that does not affect all muscle layers
o Presenting symptoms and ECG patterns often identical to UAP
o But raised cardiac enzymes due to permanent damage
ST Elevation Myocardial Infarction (STEMI): indicates prolonged coronary artery occlusion and permanent
injury
o Significant plaque rupture full thickness of myocardium affected
o ST elevation
≥ 1mm in 2 or more consecutive limb leads
Inferior leads II, III, aVF, high lateral leads I, aVL
≥ 2mm in 2 or more consecutive chest leads
Anterior leads V1-4, low lateral leads V5-6
Or new LBBB
o Later, deep Q waves represent necrotic areas of myocardium
o Reciprocal ST depression may be present
o Raised cardiac enzymes
Priorities in ACS
o Triage 1 or 2
o Early ECG and ECG review (within 5-10mins)
o GTN and aspirin if not given by ambulance
o Routine use of supplemental O2 is not recommended
O2 therapy if oxygen saturation <93% or if evidence of shock
In absence of hypoxia, benefit of O2 uncertain; may be harmful
o Full description of pain documented (PQRST)
o Possible cardiac pain and STEMI on ECG emergency revascularisation
Thrombolysis (e.g. TNK-Metalyse)
Or activate cardiac catheter lab team for primary angioplasty/stent
o Risk stratification of non-ST elevation ACS
High risk admit
Low risk monitor and d/c with upgraded medical therapy and early cardiology r/v
Treatment goals in ACS
o Decrease mortality, morbidity
o Decrease cardiac oxygen demand
o Improve or restore blood flow
o Limit infarct size
o Relieve pain and anxiety
Management of UAP/NSTEMI
o Soluble aspirin 300mg, SL GTN, IV access (avoid IM injections)
o Treatment of pain
Pain increases release of catecholamines (adrenaline, noradrenaline) increased HR,
BP, myocardial workload (risk of arrhythmias); coronary artery spasm further
ischaemia (give Morphine + Maxalon)
o Continuous cardiac monitoring and serial 12 lead ECGs
o Bedrest until pain resolved and ECG stable
Systems to support early revascularisation in STEMI
In STEMI, we aim to open an artery in less than 90minutes (door to balloon time)
Every 20 minutes saved 1% reduction in morality from AMI
Ambulance takes 12 lead ECG; if suspicious, sends ECG to closest cath lab hospital
o Emergency department
o Interventional cardiologist
o If ECG positive for STEMI, cath lab team called in and arrive with patient
In rural areas, either ambulance will give a clot busting drug (thrombolysis), or if ambulance delayed,
nurse-initiated thrombolysis will be given if required to save time and myocardium
Troponin to support diagnosis of myocardial damage
Early collection of blood for testing
Do not measure troponin (hs-TNT) unless clinical symptoms of ACS (or will get lots of false +)
If initial hs-TNT is elevated (≥ 14mg/L) or if there is a high clinical suspicion, repeat test after 3hrs
A positive finding should be followed up by a consideration of alternative, plausible explanations (e.g. PE,
aortic dissection, sepsis, chronic kidney disease) and cardiology consult if ACS suspected
Medications
Antiplatelet drugs (aspirin, clopidogrel)
Antithrombotic drugs (heparin); to reduce thrombus formation
Nitrates e.g. nitroglycerine (SL anginine, IV tridil)