ACUTE CORONARY SYNDROMES

1
ACUTE CORONARY SYNDROMES
2
Coronary Artery Disease (CAD)

• Leading cause of death in U.S.
• Decreased blood flow through coronary arteries
  myocardial ischemia/infarction
• Ischemia results from insufficient O2 supply to
  myocardium
• Atherosclerosis is leading contributor

3
CAD

• Patho
• Overgrowth of intimal smooth muscle cells with
  accumulation of macrophages and T cells
• Formation of a connective tissue matrix in the
  vessel intima
• Accumulation of lipids, esp. cholesterol, in the
  connective tissue

4
Angina Pectoris

• Strangling of the chest
• Imbalance between O2 supply and demand
• Stable Angina
• Chest discomfort occurs with increased exertion
• Limited in duration
• No permanent damage
• Relieved with rest and nitro
• Treated medically with medications

5
Angina Pectoris

• Unstable Angina
• Chest pain occurs at rest or with minimal
  exertion
• Marked limitation of activity
• Increase in number of attacks, intensity, and
  pain
• Poorly relieved with nitro
• Describes a broad spectrum of disorders
• New-onset angina, variant angina, preinfarction
  angina, and crescendo angina

6
Acute Coronary Syndromes

• Believed that atherosclerotic plaque ruptures
  causing platelet aggregation, thrombus formation,
  and vasoconstriction
• Amount of disruption of the plaque determines the
  degree of obstruction of the coronary artery and
  specific disease process
• Unstable angina
• Subendocardial MI
• MI

7
Myocardial Infarction

• Occurs when myocardial tissue is abruptly and
  severely deprived of oxygen
• Ischemia develops when blood flow is reduced
  80-90
• If blood flow is not restored, tissue necrosis
  can occur
• Most MIs result from occlusion of a coronary
  artery with atherosclerotic plaque
• Other causes include coronary artery spasm,
  platelet aggregation, and emboli from mural
  thrombi

8
Myocardial Infarction

• Often begin with infarction of subendocardial
  layer of cardiac muscle which has the greatest
  oxygen demand and the poorest oxygen supply (Zone
  of necrosis)
• Two zones surround the initial area of
  infarction
• Zone of injury (injured but not necrotic)
• Zone of ischemia (oxygen deprived)

9
Process of Infarction

• Dynamic process that evolves over several hours
• Normal conduction and contractile functions are
  suppressed by acidosis and imbalances of
  potassium, calcium, and magnesium
• Automaticity and ectopy are enhanced
• Heart rate and force of contraction are increased
  due to catecholamines released in response to
  hypoxia and pain
• Oxygen requirements increase

10
Zone of Infarction

• Actual extent of zone of infarction determined
  by
• Collateral circulation
• Anaerobic metabolism
• Workload demands on myocardium
• Injury may have occurred to the innermost layer
  (subendocardium), or
• May extend through all layers to the pericardium
  (transmural)

11
Physiologic Response to Infarction

• Will take up to six hours for obvious changes to
  occur in the heart (blue and swollen)
• After 48 hours (gray with yellow streaks)
• By 8-10 days granulation tissue forms at edges of
  necrotic tissue
• Within 2-3 months scarring develops which changes
  the shape of the left ventricle (ventricular
  remodeling)
• Remodeling may ? L ventricular function, cause
  heart failure, and ? morbidity and mortality

12
Myocardial Infarction by Location

• Response to MI depends on which coronary
  artery(ies) were obstructed and which part of the
  ventricular wall was damamge
• Anterior
• Lateral
• Septal
• Inferior
• Posterior

13
Myocardial Infarction by Location

• Anterior
• 25
• 25 mortality rate
• Likely to experience LVHF, Ventricular
  dysrhythmias
• Lateral
• 3
• Sinus Dysrhythmias
• Septal

• Inferior
• 17
• 10 mortality rate
• Bradydysrhythmias
• AV conduction delays
• 1/3 have R ventricular MI and RVHF
• Posterior
• 2
• Sinus dysrhythmias

14
Etiology of MI

• Primary factor atherosclerosis
• Non-modifiable risk factors
• Age
• Gender
• Family history
• Ethnicity

• Modifiable risk factors
• ? serum cholesterol
• Cigarette smoking
• Hypertension
• Impaired glucose tolerance
• Obesity
• Physical inactivity
• Stress

15
MI Assessment History

• Query patient about chest pain
• If experiencing acute chest discomfort, delay
  history and treat discomfort
• Obtain information about
• Management of current episode of discomfort
• Current medications
• Family history of CAD
• Presence of modifiable risk factors

16
MI Assessment Pain

• Must differentiate type of chest discomfort and
  identify source
• Query patient to determine characteristics of
  discomfort
• Onset
• Location
• Radiation
• Intensity
• Duration
• Precipitating and facilitating factors

17
MI Assessment Pain

• Remember
• angina is ischemic pain and usually improves when
  oxygen supply/demand disparity resolves.
• MI does not usually resolve with simple measures
• Associated symptoms nausea, vomiting,
  diaphoresis, dizziness, weakness, palpitations,
  and shortness of breath

18
MI Assessment Cardiovascular

• Blood pressure
• Heart rate
• Cardiac rhythm
• Distal peripheral pulses
• Skin temperature
• Heart sounds
• Respiratory rate
• Breath sounds

19
MI Assessment Psychosocial

• Denial is common early reaction
• Can be normal part of adapting to stressful event
• Detrimental if denial interferes with
  identification of symptom
• Other common reactions
• Fear
• Anxiety
• anger

20
MI Laboratory Assessment

• Cardiac Enzymes
• Creatine kinase (CK)
• CK-MB isoenzyme
• Lactic dehydrogenase (LDH)
• LDH1-LDH2
• Myoglobin
• Found in serum 2-3 hours after MI, but is not
  cardiac specific
• Always increases within 3-6 hours after MI, if
  not increased at 6 hour mark can rule out MI
• Troponin T and I
• Increased WBC

21
Cardiac Markers for MI

• Creatine Kinase (CK)
• Cardiac enzyme released after injury
• Levels rise 3-12 hours after acute MI
• Levels peak in 24 hours
• Levels to normal within 2-3 days
• MB band is specific to myocardial cells
• gt3 indicates MI

22
Cardiac Markers for MI

• Troponin
• Myocardial muscle protein released after injury
• Two subtypes T and I
• Greater sensitivity and specificity for
  myocardial injury
• Levels rise in 3-12 hours after MI
• Levels peak in 24-48 hours
• Levels back to baseline over 5-14 days
• Used for diagnostic purposes in conjunction with
  CK and the MB fraction

23
Acute MI Other Diagnostic Tests

• ECG
• Stress Test
• Thallium scans
• Multigated acquisition scan (MUGA)
• Cardiac catheterization
• (Discussed in Chapter 33)

24
ECG Changes in MI

• ST-segment elevation
• T-wave inversion
• Abnormal Q wave

25
CAD/MI Nursing Diagnoses

• Pain
• Ineffective Tissue Perfusion (cardiopulmonary)
• Activity Intolerance
• Ineffective Coping
• Fear
• Ineffective Sexuality Patterns
• Impaired Physical Mobility

26
Acute MI Collaborative Problems

• Potential for Dysrhythmias
• Potential for Heart Failure
• Potential for Recurrent Chest Discomfort and
  Extension of Injury

27
Acute MI Interventions

• Pain Management
• Review Best Practices for Managing the Client
  with Chest Discomfort Chart 38-3, p. 796
• Nitroglycerin to increase collateral blood flow,
  redistribute blood flow to subendocardium, and
  dilate coronary arteries
• Morphine Sulfate to relieve pain, decrease
  myocardial oxygen demand, and reduce circulating
  catecholamines

28
Acute MI Interventions

• Pain Management (cont)
• Supplemental O2
• 2-4 L per minute per nasal cannula
• Titrated to keep SaO2 gt 92
• Position of Comfort
• Semi-Fowlers
• Quiet and calm environment

29
Acute MI Interventions

• Thrombolytics
• Fibrinolytics dissolve clots and restore
  myocardial perfusion
• Most effective when given within 6 hours of onset
  of MI
• Client must be continuously monitored
• Contraindications Table 38-2, p. 800
• During administration monitor for bleeding and
  report any signs to physician

30
Acute MI Interventions

• Thrombolytics (cont)
• Post administration observe closely for signs of
  bleeding by
• Documenting neuro status
• Observing IV sites
• Monitoring clotting studies
• Observing for s/s of internal bleeding
• Monitor Hemoglobin and Hematocrit
• Testing stools, urine, emesis for occult blood

31
Acute MI Interventions

• Glycoprotein (GP) Inhibitors
• Target platelet component of the thrombus
• Prevent fibrinogen from attaching to activated
  platelets at the site of a thrombus
• Used in
• Acute coronary syndromes
• During and before PCTA to ensure patency
• Conjunction with fibrinolytics following MI
• During administration nurse assesses closely for
  bleeding or hypersensitivity reactions

32
Indications of Reperfusion

• Abrupt cessation of chest pain
• Sudden onset of ventricular dysrhythmias
• Resolution of ST-segment depression
• A peak at 12 hours of markers of myocardial
  damage
• Anticoagulant therapy is initiated after
  thrombolysis to maintain vessel patency

33
Acute MI Interventions

• Drug Therapy
• ASA
• Beta-adrenergic blocking agent
• ACE inhibitors
• Calcium channel blockers

34
Acute MI Interventions

• Cardiac Care Rehabilitation
• Process which assists client with cardiac disease
  to achieve and maintain optimal functioning
  within the limits of the hearts ability to
  respond to increases in activity and stress
• Phase 1 begins with acute illness, ends with
  discharge from hospital
• Phase 2 begins after discharge and continues
  through convalescence at home
• Phase 3 long term conditioning

35
Acute MI Interventions

• Cardiac Care Rehabilitation Phase 1
• Nurse promotes rest while ensuring some limited
  mobility
• Assistance is given for some ADLs
• Individualized clients progress at their own
  rate
• Nurse encourages progressive ambulation
• Nurse assesses heart rate, BP, respiratory rate
  and level of fatigue with each higher level of
  activity
• Nurse should stop the activity and refrain from
  advancing activity if client develops any signs
  of activity intolerance

36
Acute MI Interventions

• Coping
• During acute phase antianxiety agents may be
  prescribed
• Nurse assesses current coping mechanisms
• Most common are denial, anger and depression
• Denial which allows the client to minimize threat
  and use problem-focused coping mechanisms may be
  helpful in decreasing anxiety
• Anger may represent an attempt to regain control
  of life
• Depression may be the response to grief and loss
  of function

37
Acute MI Complications

• Dysrhythmias
• Heart failure
• Cardiogenic shock
• Recurrent chest discomfort and extension of injury

38
Dysrhythmias

• Cause of death in clients with MI who die prior
  to hospitalization
• 70-90 of hospitalized MI clients have abnormal
  cardiac rhythms
• Identify the dysrhythmia
• Assess hemodynamic status
• Evaluate client for chest discomfort
• Treated when they cause
• Hemodynamic compromise
• Increased myocardial oxygen requirements
• Predispose lethal ventricular dysrhythmias

39
Dysrhythmias

• Inferior MI
• Bradycardias
• 2nd Degree AV Blocks
• Transient
• Nurse monitors
• Cardiac rate rhythm
• Hemodynamic status
• May need temporary pacer if hemodynamically
  unstable

• Anterior MI
• Venrticular irritability (PVCs)
• 3rd Degree or Bundle Branch Block (serious
  complication)
• Nurse observes closely for s/s of heart failure
• May need pacemaker

40
Heart Failure

• Relatively common complication
• May result from
• Left ventricular dysfunction
• Rupture of the intraventriculal septum
• Papillary muscle rupture with valvular
  dysfunction
• Right ventricular infarction
• Cardiogenic Shock is the most severe form
• Accounts for most in-hospital deaths after MI

41
Heart Failure

• Assessments and Interventions
• Ascultate for crackles
• Be alert for development of wheezing, tachypnea,
  and frothy sputum
• Ascultate heart sounds, take note of S3
• Monitor for signs of poor organ perfusion
• Hemodynamic monitoring

42
Heart Failure

• Signs of Poor Organ Perfusion
• Change in orientation or mental status
• Urine output less than 1mL/kg/hr or less than 30
  mL/hr
• Cool, clammy extremities with decreased or absent
  pulses
• Unusual fatigue
• Recurrent chest pain

43
Classification of Post-MI Heart Failure

• See chart 38-3 p. 803 Killip Classification of
  Heart Failure
• Class I responds well to reduction in preload
  with IV diuretics
• Class II and III require IV diuretics and meds to
  reduce afterload or enhance contractilty
• Positive inotropes are useful but can increase
  cardiac oxygen consumption resulting in further
  decreased CO
• Class IV is a medical emergency requiring early
  identification and prompt treatment

44
Cardiogenic Shock

• Tachycardia
• Hypotension
• Blood pressure less than 90 mmHg, or 30 mmHg less
  than clients baseline
• Urine output less than 30 mL/hr
• Cole, clammy skin with poor peripheral pulses
• Agitation, restlessness, confusion
• Pulmonary congestion
• Tachypnea
• Continuing chest discomfort

45
Heart Failure Medical Management

• Goal is to relieve pain and decrease myocardial
  oxygen consumption
• IV morphine
• Oxygen
• Medications to improve tissue perfusion, decrease
  workload of heart and increase cardiac
  contractility
• Intra-Aortic Balloon Pump (Figure 38-4, p. 805)
  may be used when drug therapy is ineffective

46
Intra-Aortic Balloon Pump

• Invasive intervention to improve myocardial
  perfusion during an acute MI, reduce afterload,
  and facilitate emptying of the left ventricle
• Balloon inflates during diastole to increase
  diastolic pressure and improve perfusion
• Balloon deflates just before systole reduces
  afterload at the time of systolic contractions to
  facilitate emptying of the left ventricle thus
  improving CO

47
Potential for Recurrent Chest Pain and Extension
of Injury

• Recurrent chest discomfort (pain) is one of the
  major indicators for surgical intervention
• Goal to resolve angina or prevent MI
• Management
• Percutaneous Transluminal Coronary Angioplasty
• Coronary Artery Bypass Graft

48
PTCA Percutaneous Transluminal Coronary
Angioplasty

• Invasive, but nonsurgical technique to reduce
  frequency and severity of chest discomfort
• Complexity and location assessed to determine
  whether client would benefit from procedure
• May also be used during evolving MI
• Procedure performed under fluoroscopic guidance
  in cardiac cath lab
• Balloon inflation may be repeated until lesion is
  reduced or eliminated
• Meds include heparin, nitriglycerine or
  nifedipine
• Stents may be placed at time of procedure

49
PTCA Post-Procedure Care

• Monitor for potential problems
• Acute closure of the vessel
• Bleeding from insertion site
• Reaction to the dye
• Hypotension
• Hypokalemia
• dysrhythmias

• Drug Therapy
• Long term nitrate
• Calcium channel blockers
• ASA
• Beta blocker and ACE inhibitor may be added
• Glycoprotein inhibitors during initial hours
• Potassium supplements if indicated
• Coagulation with coumadin

50
Coronary Artery Bypass Graft

• Most common cardiac surgery
• Indicated for clients who do not respond to
  medical management of CAD or when disease
  progression is evident
• To be bypassed vessels should have proximal
  lesions with gt 70 occlusion
• Most effective when good ventricular function
  remains and ejection fraction is more than 40-50
• Requires Cardiopulmonary bypass during surgery

51
CABG Post-Op Care

• Mechanical ventilation for 3-6 hours
• Mediastinal tubes to waterseal drainage
• Epicardial pacing wires
• Hemodynamic monitoring
• Observes closely for
• Dysrhythmias (ventricular ectopics,
  bradydysrhythmias, or heart block)
• Fluid and electrolyte imbalances (K at 4-5)
• Hypotension, hypothermia, hypertension
• Cardiac tamponade
• Altered cerebral perfusion

52
Cardiac Tamponade

• Blood accumulates around the heart
• Medical emergency
• Hallmarks in post-CABG patient
• Sudden cessation of previously heavy mediastinal
  drainage
• JVD with clear lung sounds
• Pulsus paradoxus
• Equalization of PAWP and right artrial pressure

53
Neurological Changes Post-CABG

• Transient
• 75 transient changes due to
• Anesthesia, CPB, air emboli, hypothermia
• Experience
• Slowness to arouse
• Memory loss
• confusion
• Usually return to baseline in 4-8 hours

• Permanent
• Changes may be associated with stroke during
  surgery
• Experience
• Abn. pupillary response
• Failure to awaken from anesthesia
• Seizures
• Absence of sensory or motor function
• Monitor
• Neuro status q 30-60 min initially then q 2-4
  hours

54
Additional Interventions

• Minimally Invasive Direct Coronary Artery Bypass
  (MIDCAB)
• May be indicated for lesion of left anterior
  descending artery
• Transmyocardial Laser Revascularization
• Indicated for unstable angina and inoperable CAD
  with areas of reversible myocardial ischemia
• Laser creates narrow channels through left
  ventricular muscle to the left ventricle to allow
  oxygenated blood flow from the ventricle to the
  muscle during diastole