Acute Coronary Syndromes And Nursing Role

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Epidemiology

– Ischemic heart dx is the main cause of death in developed countries

  • 30% of male deaths
  • 20% of female
  • In the UK

– Incidence increases with age, male sex, and postmenopause in women

Risk factors:

  • Hypertension
  • Hypercholesterolemia
  • Cigarette smoking
  • Family history
  • diabetes

 

Pathogenesis  of Acute Coronary Syndromes

  • MI results from an imbalance between oxygen supply and demand
  • Stable angina (chest pain) is caused by narrowing of coronary arteries by smooth plaque without overlying thrombosis
  • Unstable angina occurs when small, non-occlusive complex plaques with lipid-rich cores and fibrous caps rupture under stress causing overlying thrombus and vasospasm
  • If untreated, unstable angina can progress to an MI or sudden cardiac death
  • MI is due to fresh occlusive coronary artery thrombus overlying atherosclerotic lesions
  • MI with normal coronary arteries is rare but can follow vasospasms or cocaine abuse

 

Factors that limit oxygen supply

  • Coronary artery narrowing
  • Atherosclerosis
  • Vasospasm
  • Complex plaques
  • Reduced coronary artery flow
    • Hypotension
    • Decreased diastolic time
    • LV hypertrophy
    • Increased LV end-diastolic pressure
  • Reduced oxygen carrying capacity
    • Hypoxemia
    • anemia

     

    Factors that increase oxygen demand

    • Increased HR
    • Exercise
    • Tachycardia
  • Increased LV afterload and mass
    • Increased myocardial wall stress
    • Hypertension
    • Aortic stenosis
  • Increased RV afterload
    • Pulmonary embolism
    • Pulmonary hypertension
  • Increased contractility
    • thyrotoxicosis

     

    Clinical Features of MI

    • Crushing, heavy substernal chest pain radiating to the neck and medial aspect of the left arm
    • Pain may be atypical (like a burning), localized (only in the jaw), or absent
    • Stable angina is usually caused by exercise or anxiety, is short-lived, and is relieved by rest and/or NTG
    • Unstable angina occurs at rest and lasts longer…new pain, altered stable angina pattern, nausea/sweating, and radiation to new sites also suggests unstable angina
    • Myocardial infarction signs/symptoms
    • Abrupt onset of severe, prolonged pain
    • Autonomic symptoms (sweating, nausea)
    • Dyspnea
    • Anxiety
    • Tachycardia or bradycardia, depending on site of MI
    • Hypotension
    • Gallop heart rhythm

     

    Complications of MI

    • Arrhythmias
    • Papillary muscle or free wall rupture
    • Pericarditis
    • Ventricular septal defects
    • Heart failure

     

    Determining/confirming an MI

    Serial EKG’s

    • Angina
    • T wave inversion
    • ST depression
    • Conduction defects (eg-bundle branch blocks)

    MI

    • Subendocardial (doesn’t go all the way thru the muscle)
    • ST depression
    • T wave inversion
  • Transmural (goes all the way thru the muscle)
    • Presence of Q wave
    • Elevated ST segment

    Cardiac enzymes

    • Myocardial necrosis releases cardiac enzymes into the plasma…CTT and CK-MB peak within 24 hours…LDH-1 peaks at ~3-4 days out
    • Increased cardiac troponin T (CTT) at 12 hrs makes diagnosis
    • Increased LDH-1suggests late presentation MI
    • Doubling of baseline CK-MB confirms MI

    Blood tests

    • WCC
    • Blood glucose
    • ESR

    Echocardiography

    • May show dyskinesia of muscle, mural thrombus, perforations, aneurysms, papillary muscle rupture, and valve lesions

    Nuclear scans

    • Technetium pyrophosphate
    • Concentrates in area of damage
  • Thallium scans
    • Show cold spots in non-perfused myocardium and demonstrate areas of reversible ischemia

    Management of unstable angina

    Antianginal therapy

    • Reduces myocardial oxygen consumption by lowering heart rate and afterload
    • Bed rest
    • Beta blockers
    • Antihypertensives
  • increases myocardial oxygen supply using oxygen and pharmacotherapy
  • Coronary artery dilation – nitrates
    • Also decrease LV wall tension by reducing preload and afterload
  • Relieve vasospasm – calcium channel blockers
    • Negative inotropes and may cause tachycardia

    Antithrombotic therapy

    • Aspirin prevents platelet aggregation within 15 min reducing the risk of MI and death
    • Antiplatelet agents can be useful but have a slow onset (eg-Plavix)
    • IV heparin, in combo with ASA, reduces morbidity and mortality
    • Thrombolytics do not reduce MI or mortality with unstable angina

    Early revascularization (angioplasty) does not improve outcome

     

    Management and Nursing role of MI

    • Early reperfusion and minimizing myocardial oxygen consumption limits infarction size and reduces mortality
    • Acute management
    • Bed rest
    • Cardiac monitoring
    • Oxygen (>60%?)
    • Sublingual nitrites reduce pain
    • Opiates relieve pain and decrease O2 consumption
    • Early beta blockade limits infarct size, arrhythmias, and mortality
    • Oral ACE inhibitors improve LV remodelling and reduce heart failure
    • Prophylactic subQ heparin prevents thromboembolic complications
  • Thrombolytic therapy
    • Breaks down clots, reperfuses ischemic tissue, limits damage, and reduces complications
    • Most effective if given within 3 hours
    • Accelerates conversion of plasminogen to plasmin, an enzyme that attacks fibrin
    • Increases the risk of hemorrhage
    • Streptokinase can only be used once as it causes allergic reactions
    • TPA only activates plasminogen that is bound to fibrin, so it’s better targeted than other thrombolytics

     

    Contraindications to thrombolytic

    Absolute

    Active bleeding, aortic dissection, neurosurgery, head injury, recent CNS dx, CVA, recent operation, recent trauma, diastolic hypertension, coagulopathy

    Relative

    Previous CVA or TIA, recent prolonged CPR, systolic hypertension, recent non-compressible central lines, intracardiac thrombus, abdominal aortic aneurysm

     

    Percutaneous coronary angioplasty (PTCA)

    Primary

    • Used instead of thrombolytics to open coronary arteries
    • Done within 6 hours of symptoms

    Rescue

    • Used if thrombolytics aren’t successful

    Ongoing management

    • Reduce risk factors
    • Angiography/early revascularization
    • Warfarin (Coumadin) for 3 months
    • ASA indefinatelylB-blockers/ACE inhibitors up to 1 year

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