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Coronary artery disease
A blood vessel disorder that is included in
atherosclerosis
cause
• Atherosclerosis ; characterized by focal deposit of
cholesterol and lipids within the arterial wall
Predisposing factors
• Age and gender
• Occurs in men between 35 to 45 years age
• After the age of 65 incidence of women and men
equalizes
• heredity
• Genetic pre-disposition but actual mechanism is
unknown
• Diabetes; 2-3 times more in diabetes ;
• maybe due to circulating insulin helps to form
atheroma and damaged arterial intima and insulin
modifies lipid metabolisms
• Hypertension
• Smoking and tobacco use (nicotine)
• Sedentary lifestyle
• Obesity
• Stress and behavior pattern
Major clinical manifestations
• Angina pectoris
• Myocardial infarction
• Hidden cardiac death
Angina pectoris
• pain (angina) in the chest (pectoris)
• ANGINA PECTORIS is defined as transient chest pain
caused by myocardial ischaemia
• Usually lasts for 3-5 minutes
• commonly subsides when the precipitating factor
(usually exertion) is relieved
Etiology
• Myocardial ischaemia develops when the demand
for myocardial oxygen exceeds the ability of the
coronary arteries to supply it.
• Primary reasons for insufficient blood flow is
narrowing of coronary arteries by atherosclerosis
• Extracardiac factors may precipitate myocardial
ischaemia and anginal pain
• Physical exertion
• Strong emotions
• Consumption of heavy meal
• Temperature extremes
• Cigarette smoking
• Sexual activity
• Stimulants such as cocaine
Pathophysiology
• Coronary artery disease refers to the development
and progression of plague accumulation in
coronary arteries.
• This process has three stages along; stable angina,
unstable angina and myocardial infarction
Clinical manifestation
• The following may occur with stable angina,
unstable angina and acute MI
• Chest pain or anginal equivalent(jaw pain, left arm
pain
• Non-verbal indicators of pain: clutch, rub, stroke on
the chest
• Increase or decrease in heart rate,
• dysrhythmias,
• Increase or a decrease in blood pressure
• Angina that occurs with predictable level of
exertion (stable angina)
• Angina not necessarily associated with activity and
ST depression (ECG)
In addition to unique features of
myocardial infarction
• Angina not relieved by rest or nitroglycerin therapy
• Associated with symptoms: dizziness, dyspnoea,
nausea, vomiting, feeling of impending doom
• Altered neurological status, if decreased cardiac
output
• Rales if decreased contractility creates left
ventricular function
• Presence of s3 (heard early in diastole)
• s4 (occurs late in diastole) gallop
• Diminished pulses
• Pallor
• ECG ST elevation
• Elevated ESR
Treatment Guidelines for acute
Myocardial infarction
• Use rapid transport to hospital
• Obtain 12 –lead electrocardiogram to be read
within 10 minutes
• Obtain laboratory blood specimens of cardiac
biomarkers including troponin
• Obtain other diagnostics to clarify the diagnosis
• Begin routine medical interventions
• Supplemental oxygen
• Nitroglycerin
• Morphine to reduce pain and anxiety also reduces
preload and afterload hence decreasing work of the
heart
• Aspirin 162-325mg to prevent clot formation
• Beta –blocker incase of dysrhythmias , within 24hrs
• Angiotensin-converting enzyme inhibitor within 24
hours prevent conversion of angiotensin 1 to
angiotensin 11
• Anticoagulation with heparin and platelet inhibitors
• Evaluate for indications for re-perfusion therapy
• Percutaneous coronary intervention
• Thrombolytic (fibrinolytic) therapy –alteplase
(activase) to dissolve thrombus
• Continue therapy as indicated
• Iv heparin, low molecular weight heparin-
bivalirudin, fondaparinux
• Clopidogrel (Plavix)
• Glycoprotein 11b/111a inhibitor
• Bed rest for a minimum of 12-24hours
Pt monitoring
• Blood pressure
• Urine output
• Serum sodium, potassium and cretinine levels
Cardiac rehabilitation
• Reassure the pt as CAD is a lifelong disease
• Advise on recommended activity which should
depend on; pt’s age,
• condition before the cardiac event,
• the extent of the disease
• the course of hospital stay
• the development of any complications
Nursing care
• Pt’s systemic assessment- take hx on S&S
• To include; chest pain or discomfort, difficulty
breathing, palpitations, unusual fatigue, faintness
(syncope)
• A focused physical assessment to detect
complications and detect any change in pt status
• Two iv lines are placed for administering emergency
medications
• Iv lines are changed to saline lock to maintain IV
access
Assignment
• Draw a nursing care plan for this patient
Potential complications
• Acute pulmonary edema
• Heart failure
• Cardiogenic shock
• Dysrhythmias and cardiac arrest
• Pericardial effusion
• Cardiac tamponade

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cvs-Coronary artery disease.pptx

  • 1. Coronary artery disease A blood vessel disorder that is included in atherosclerosis
  • 2. cause • Atherosclerosis ; characterized by focal deposit of cholesterol and lipids within the arterial wall
  • 3. Predisposing factors • Age and gender • Occurs in men between 35 to 45 years age • After the age of 65 incidence of women and men equalizes • heredity • Genetic pre-disposition but actual mechanism is unknown
  • 4. • Diabetes; 2-3 times more in diabetes ; • maybe due to circulating insulin helps to form atheroma and damaged arterial intima and insulin modifies lipid metabolisms • Hypertension • Smoking and tobacco use (nicotine) • Sedentary lifestyle
  • 5. • Obesity • Stress and behavior pattern
  • 6. Major clinical manifestations • Angina pectoris • Myocardial infarction • Hidden cardiac death
  • 7. Angina pectoris • pain (angina) in the chest (pectoris) • ANGINA PECTORIS is defined as transient chest pain caused by myocardial ischaemia • Usually lasts for 3-5 minutes • commonly subsides when the precipitating factor (usually exertion) is relieved
  • 8. Etiology • Myocardial ischaemia develops when the demand for myocardial oxygen exceeds the ability of the coronary arteries to supply it. • Primary reasons for insufficient blood flow is narrowing of coronary arteries by atherosclerosis • Extracardiac factors may precipitate myocardial ischaemia and anginal pain
  • 9. • Physical exertion • Strong emotions • Consumption of heavy meal • Temperature extremes • Cigarette smoking • Sexual activity • Stimulants such as cocaine
  • 10. Pathophysiology • Coronary artery disease refers to the development and progression of plague accumulation in coronary arteries. • This process has three stages along; stable angina, unstable angina and myocardial infarction
  • 11. Clinical manifestation • The following may occur with stable angina, unstable angina and acute MI • Chest pain or anginal equivalent(jaw pain, left arm pain • Non-verbal indicators of pain: clutch, rub, stroke on the chest • Increase or decrease in heart rate, • dysrhythmias,
  • 12. • Increase or a decrease in blood pressure • Angina that occurs with predictable level of exertion (stable angina) • Angina not necessarily associated with activity and ST depression (ECG)
  • 13. In addition to unique features of myocardial infarction • Angina not relieved by rest or nitroglycerin therapy • Associated with symptoms: dizziness, dyspnoea, nausea, vomiting, feeling of impending doom • Altered neurological status, if decreased cardiac output • Rales if decreased contractility creates left ventricular function
  • 14. • Presence of s3 (heard early in diastole) • s4 (occurs late in diastole) gallop • Diminished pulses • Pallor • ECG ST elevation • Elevated ESR
  • 15. Treatment Guidelines for acute Myocardial infarction • Use rapid transport to hospital • Obtain 12 –lead electrocardiogram to be read within 10 minutes • Obtain laboratory blood specimens of cardiac biomarkers including troponin • Obtain other diagnostics to clarify the diagnosis • Begin routine medical interventions
  • 16. • Supplemental oxygen • Nitroglycerin • Morphine to reduce pain and anxiety also reduces preload and afterload hence decreasing work of the heart • Aspirin 162-325mg to prevent clot formation • Beta –blocker incase of dysrhythmias , within 24hrs • Angiotensin-converting enzyme inhibitor within 24 hours prevent conversion of angiotensin 1 to angiotensin 11 • Anticoagulation with heparin and platelet inhibitors
  • 17. • Evaluate for indications for re-perfusion therapy • Percutaneous coronary intervention • Thrombolytic (fibrinolytic) therapy –alteplase (activase) to dissolve thrombus • Continue therapy as indicated • Iv heparin, low molecular weight heparin- bivalirudin, fondaparinux • Clopidogrel (Plavix)
  • 18. • Glycoprotein 11b/111a inhibitor • Bed rest for a minimum of 12-24hours
  • 19. Pt monitoring • Blood pressure • Urine output • Serum sodium, potassium and cretinine levels
  • 20. Cardiac rehabilitation • Reassure the pt as CAD is a lifelong disease • Advise on recommended activity which should depend on; pt’s age, • condition before the cardiac event, • the extent of the disease • the course of hospital stay • the development of any complications
  • 21. Nursing care • Pt’s systemic assessment- take hx on S&S • To include; chest pain or discomfort, difficulty breathing, palpitations, unusual fatigue, faintness (syncope) • A focused physical assessment to detect complications and detect any change in pt status • Two iv lines are placed for administering emergency medications
  • 22. • Iv lines are changed to saline lock to maintain IV access
  • 23. Assignment • Draw a nursing care plan for this patient
  • 24. Potential complications • Acute pulmonary edema • Heart failure • Cardiogenic shock • Dysrhythmias and cardiac arrest • Pericardial effusion • Cardiac tamponade

Editor's Notes

  1. Acute pain related to increased myocardial oxygen demand and decreased myocardial oxygen supply Acute pain related to increased myocardial oxygen demand and decreased myocardial oxygen