CORONARY ARTERY DISEASE

1. CORONARY ARTERY DISEASE OXYGENATION/ PERFUSION NEEDS Nursing Management Coronary Artery Disease Lewis Ch 34 Chapter 32 5th edition, Chapter 33 in 6th editionChapter 32 5th edition, Chapter 33 in 6th edition

4. Coronary Artery Disease Significance Number one cause of death in US. Myocardial infarction increased in those > 60 years Etiology/Pathophysiology starts with endothelial injury (HTN, hyperlipid) platelet activation, release of growth factor growth of smooth muscle Death rate decreased by 30% 1985-1995 CAD also known as: CVHD, ischemic HD, coronary HD plaque forms, atheromatous deposits lead to coronary occlusion when thrombus occursDeath rate decreased by 30% 1985-1995 CAD also known as: CVHD, ischemic HD, coronary HD plaque forms, atheromatous deposits lead to coronary occlusion when thrombus occurs

5. Coronary Artery Disease lipids trapped in tissue calcification begins Developmental stages of plaque fatty streak fibrous plaque complicated lesion fatty streaks seen as early as age 15 fibrous plaque at age 30, particularly if smoking, hyperlipidemia lesion has lipid center, surrounded by necrosis and calcium deposits Table 32-1 p. 843 and 33-1 p. 800fatty streaks seen as early as age 15 fibrous plaque at age 30, particularly if smoking, hyperlipidemia lesion has lipid center, surrounded by necrosis and calcium deposits Table 32-1 p. 843 and 33-1 p. 800

6. Description A type of blood vessel disorder that is included in the general category of atherosclerosis Atherosclerosis Begins as soft deposits of fat that harden with age Referred to as the �hardening of arteries� Can occur in any artery in the body Atheromas (fatty deposits) Preference for the coronary arteries

7. Description Atherosclerosis Terms to describe the disease process: Arteriosclerotic heart disease (ASHD) Cardiovascular heart disease (CHD) CAD Cardiovascular diseases are the major cause of death in the United States Heart attacks are still the leading cause of all cardiovascular disease deaths and deaths in general

8. Etiology and Pathophysiology Atherosclerosis is the major cause of CAD Characterized by a focal deposit of cholesterol and lipids, primarily within the intimal wall of the artery Endothelial lining altered as a result of chemical injuries Hyperlipidemia Hypertension C-reactive protein (CRP) Nonspecific marker of inflammation Increased in many patients with CAD Chronic exposure to CRP triggers the rupture of plaques

9. Etiology and Pathophysiology Endothelial alteration ? Platelets are activated Growth factor stimulates smooth muscle proliferation Endothelial alteration ? Cell proliferation entraps lipids, which are calcified over time and form an irritant to the endothelium on which platelets adhere and aggregate Endothelial alteration ? Thrombin is generated Fibrin formation and thrombi occur

12. Etiology and PathophysiologyDevelopmental Stages Fatty streak Earliest lesions Characterized by lipid-filled smooth muscle cells Yellow tinge appears Reversible Raised fibrous plaque Beginning of progressive changes in the arterial wall Initiated by chronic endothelial injury

13. Etiology and PathophysiologyDevelopmental Stages Complicated lesion Final stage in development The most dangerous Plaque consists of a core of lipid materials within an area of dead tissue With the incorporation of lipids, thrombi, damaged tissue, and accumulation of calcium, the growing lesion becomes complex

14. Etiology and PathophysiologyCollateral Circulation Normally some arterial branching, termed collateral circulation, exists within the coronary circulation

15. Etiology and PathophysiologyCollateral Circulation Growth of collateral circulation is attributed to two factors: The inherited predisposition to develop new vessels The presence of chronic ischemia When occlusion of the coronary arteries occurs slowly over a long period, there is a greater chance of adequate collateral circulation developing

16. Collateral Circulation

17. Non-denuding injury (hyperlipidemia) smooth muscle proliferation with increased collagen and fibrin Denuding injury (shear forces, HTN) when complicated lesion ruptures? Platelets and thrombin rush in. Activation of platelets causes release of glycoprotein IIB/IIIA which leads to binding of fibrinogen.Non-denuding injury (hyperlipidemia) smooth muscle proliferation with increased collagen and fibrin Denuding injury (shear forces, HTN) when complicated lesion ruptures? Platelets and thrombin rush in. Activation of platelets causes release of glycoprotein IIB/IIIA which leads to binding of fibrinogen.

19. Coronary Artery Disease Collateral circulation Risk Factors: Unmodifiable age gender race genetic inheritance Risk factors originally based on Framingham study: all people studied in town (> 5000 men and women for 20 years) Unmodifiable risk factors are those that cannot be changed. Increased incidence Caucasian, middle aged men. But�after age 60 women have nearly equal incidence CAD Women have higher incidence at a younger age if: CIGARETTE SMOKING, stress, HTN, oral contraceptives Native Americans less than 35 years associated with obesity, DM. 2X mortality rate of others African American males with higher incidence HTN actually at less risk but more severe disease when it occurs. Hispanics: lower death rates Asians: less incidence but more when compared to countries of origin.Risk factors originally based on Framingham study: all people studied in town (> 5000 men and women for 20 years) Unmodifiable risk factors are those that cannot be changed. Increased incidence Caucasian, middle aged men. But�after age 60 women have nearly equal incidence CAD Women have higher incidence at a younger age if: CIGARETTE SMOKING, stress, HTN, oral contraceptives Native Americans less than 35 years associated with obesity, DM. 2X mortality rate of others African American males with higher incidence HTN actually at less risk but more severe disease when it occurs. Hispanics: lower death rates Asians: less incidence but more when compared to countries of origin.

20. Coronary Artery Disease (CAD) Risk factors: Modifiable elevated serum lipids (major) hypertension (major) Tobacco use (major) obesity (major) sedentary life style (major) Contributing factors diabetes mellitus stress/behavioral patterns Fasting serum cholesterol > 200 mg., triglycerides > 150, LDL >130 and HDL <45. B/P > 140/90 shearing forces cause denuding injury and heart must work harder to pump. Body response is to retain fluid to improve blood flow. Fluid then increases the workload of the heart. ( lower Na+ intake) smoking especially risky for women. Nicotine increases catecholamines > increased HR, BP and peripheral vasoconstriction> increased cardiac workload. Carbon monoxide competes for oxygen-carrying sites on Hgb molecule, makes less oxygen available. obesity with wt > 30% IBW Physical inactivity leads to lowered HDL, less development of collaterals, oxygen use not efficientFasting serum cholesterol > 200 mg., triglycerides > 150, LDL >130 and HDL <45. B/P > 140/90 shearing forces cause denuding injury and heart must work harder to pump. Body response is to retain fluid to improve blood flow. Fluid then increases the workload of the heart. ( lower Na+ intake) smoking especially risky for women. Nicotine increases catecholamines > increased HR, BP and peripheral vasoconstriction> increased cardiac workload. Carbon monoxide competes for oxygen-carrying sites on Hgb molecule, makes less oxygen available. obesity with wt > 30% IBW Physical inactivity leads to lowered HDL, less development of collaterals, oxygen use not efficient

21. Coronary Artery Disease (CAD) Risk factors: Modifiable elevated homocysteine levels elevations highly sensitive C reactive protein indicates inflammatory response homocysteine is associated with CAD. B-complex supplements can cause 16% reduction in venous thrombosis.homocysteine is associated with CAD. B-complex supplements can cause 16% reduction in venous thrombosis.

22. LDL, VLDL transport cholesterol and lipids to blood vessel walls (macrophages become cholesterol foam cells.) HDL removes cholesterol, transporting it to the liver where it is metabolized and then excreted in bile. Can cholesterol be totally eliminated if 0 intake? No, made in liver. Triglycerides are associated with obesity, sedentary life style, high ETOH intake. Lipoproteins: soluble fat bound to protein HDL: higher with estrogen and physical activity, decreases after menopause. (HDL2, HDL3) LDL contains the most cholesterol, loves arterial walls and elevation associated with worsening atherosclerosis. VLDL contains triglycerides. Increased in those with premature atherosclerosis, particularly if smoke, HTN.LDL, VLDL transport cholesterol and lipids to blood vessel walls (macrophages become cholesterol foam cells.) HDL removes cholesterol, transporting it to the liver where it is metabolized and then excreted in bile. Can cholesterol be totally eliminated if 0 intake? No, made in liver. Triglycerides are associated with obesity, sedentary life style, high ETOH intake. Lipoproteins: soluble fat bound to protein HDL: higher with estrogen and physical activity, decreases after menopause. (HDL2, HDL3) LDL contains the most cholesterol, loves arterial walls and elevation associated with worsening atherosclerosis. VLDL contains triglycerides. Increased in those with premature atherosclerosis, particularly if smoke, HTN.

23. CAD: Health promotion and maintenance Modifiable risk factor management Nutrition normalize weight diet low in saturated fats, cholesterol Pharmacologic management Drugs that increase removal lipoproteins resin-type drugs: cholestyramine, colestipol Drugs that decrease production of lipoproteins HMG-CoA reductase inhibitors or �statins� lovastatin (Mevacor), atorvastatin (Lipitor)

24. CAD: Health promotion and maintenance Drugs that decrease production of lipoproteins nicotinic acid gemfibrozil clofibrate Drugs which decrease absorption of cholesterol ezetimibe (Zetia) Zetia inhibits dietary AND biliary cholesterol from being absorbed in the intestine Many new indicators of hyperlipidemia currently being tested. Zetia inhibits dietary AND biliary cholesterol from being absorbed in the intestine Many new indicators of hyperlipidemia currently being tested.

25. CAD: Health promotion and maintenance When are drugs started? try dietary modification and exercise first 6 months drugs typically taken for the rest of one�s life to keep lipids under control. Read dietary management and be able to recognize appropriate diet. Red meat, dairy. Eggs?Read dietary management and be able to recognize appropriate diet. Red meat, dairy. Eggs?

27. Clinical Manifestations of CAD Angina Pectoris Acute Coronary Syndrome Sudden Cardiac Death

28. Clinical Manifestations Stable Angina Results when the lack of oxygen supply is temporary and reversible Acute Coronary Syndrome (ACS) Develops when the oxygen supply is prolonged and not immediately reversible ACS encompasses: Unstable angina Non-ST-segment-elevation myocardial infarction (NSTEMI) ST-segment-elevation (STEMI)

29. CAD: Clinical Manifestations Angina pectoris when demand exceeds supply of myocardial oxygen? ISCHEMIA usually due to insufficient flow of oxygenated blood narrowed arteries coronary spasm cellular metabolism changes to anaerobic and causes buildup of lactic acid which irritates nerves and transmits pain to cardiac nerves and thoracic nerve roots. Transient, < 20 min. chest pain, typically relieved by rest. Which part of the heart does most work? Left ventricle. With rising diastolic pressure, must work harder. Cellular metabolism changes: cyanotic in 10 sec., changes ECG, < contractility, no glucose to cells> anaerobic metabolism>lactic acid produced> irritation nerves>pain in some. Myocardium efficiently removes 60-85% available oxygen. Will first try dilating vessels (ASHD, HTN, smoking?) If spasm? temporary constriction, reversible. Usually associated with plaque. CCBs prescribed. Time of blockage determines outcome: ischemia vs. infarction. Twitchy, irritable myocardium�Transient, < 20 min. chest pain, typically relieved by rest. Which part of the heart does most work? Left ventricle. With rising diastolic pressure, must work harder. Cellular metabolism changes: cyanotic in 10 sec., changes ECG, < contractility, no glucose to cells> anaerobic metabolism>lactic acid produced> irritation nerves>pain in some. Myocardium efficiently removes 60-85% available oxygen. Will first try dilating vessels (ASHD, HTN, smoking?) If spasm? temporary constriction, reversible. Usually associated with plaque. CCBs prescribed. Time of blockage determines outcome: ischemia vs. infarction. Twitchy, irritable myocardium�

30. CAD: Angina Precipitating factors physical exertion (? heart rate) strong emotions (? catecholamines) consumption of a heavy meal (blood diverted) temperature extremes cigarette smoking sexual activity stimulants (cocaine, caffeine) circadian rhythm patterns temperature extremes: dilation, constriction of vessels cigarette smoking increases heart rate, decreases oxygen sexual activity sympathetic stimulation Circadian early AM after awakening. Other causes of myocardial oxygen imbalance: hypotension including shock, vasoconstricting drugs, cardiac valve disorders (>HR), CHF, anemia, chronic lung diseasetemperature extremes: dilation, constriction of vessels cigarette smoking increases heart rate, decreases oxygen sexual activity sympathetic stimulation Circadian early AM after awakening. Other causes of myocardial oxygen imbalance: hypotension including shock, vasoconstricting drugs, cardiac valve disorders (>HR), CHF, anemia, chronic lung disease

31. CAD: Angina Types of angina stable unstable (USA) or acute coronary syndrome AKA progressive, crescendo, pre-infarction angina variant or Prinzmetal�s nocturnal angina? Clinical manifestations Pain: squeezing, cramping, choking, burning stable: typical onset, duration, intensity; usually caused by exercise unstable: fits in acute coronary syndrome spectrum and may progress due to MI. Hospitalize. Most due to rupture of previously stable plaque. Pain: 80% don�t feel. Often silent in diabetes, HTN Prinzmetal�s: often @ rest during REM, more common in hx. of migraine, Raynaud�s, associated with spasm.stable: typical onset, duration, intensity; usually caused by exercise unstable: fits in acute coronary syndrome spectrum and may progress due to MI. Hospitalize. Most due to rupture of previously stable plaque. Pain: 80% don�t feel. Often silent in diabetes, HTN Prinzmetal�s: often @ rest during REM, more common in hx. of migraine, Raynaud�s, associated with spasm.

32. Types of AnginaStable Angina Pectoris Chest pain occurring intermittently over a long period with the same pattern of onset, duration, and intensity of symptoms Pain usually lasts 3 to 5 minutes Subsides when the precipitating factor is relieved Pain at rest is unusual ECG reveals ST segment depression Stable angina can be controlled with medications on an outpatient basis

33. Canadian Cardiovascular Society Angina Classification Class 0: Asymptomatic Class 1: Angina with strenuous Exercise Class 2: Angina with moderate exertion Class 3: Angina with mild exertion Walking 1-2 level blocks at normal pace Climbing 1 flight of stairs at normal pace Class 4: Angina at any level of physical exertion

34. Types of AnginaSilent Ischemia Up to 80% of patients with myocardial ischemia are asymptomatic Associated with diabetes mellitus and hypertension

35. Types of AnginaPrinzmetal�s Angina �Variant angina� Occurs at rest usually in response to spasm of major coronary artery Seen in patients with a history of migraine headaches and Raynaud�s phenomenon Spasm may occur in the absence of CAD When spasm occurs: Pain Marked, transient ST segment elevation May occur during REM sleep

36. Types of AnginaNocturnal Angina and Angina Decubitus Nocturnal Angina Occurs only at night but not necessarily during sleep Angina Decubitus Chest pain that occurs only while lying down Relieved by standing or sitting

37. Types of AnginaUnstable Angina Angina that is: New in onset Occurs at rest Has a worsening pattern Unpredictable Considered to be an acute coronary syndrome Associated with deterioration of a once stable atherosclerotic plaque

38. Clinical Manifestations Angina Most common clinical manifestation is chest pain or discomfort Exact cause of the pain is unknown Neurogenic pain at the site of ischemia is most likely Referred to as a vague sensation, a strange feeling, pressure, or ache in the chest An unpleasant feeling described as constrictive, squeezing, heaving, choking, or suffocating sensation Almost never sharp or stabbing Usually does not change with position or breathing May complain of severe indigestion or burning

39. Treatment/Education for Stable Angina A-ASA and antianginal therapy- nitro imdur B-Beta Blocker and Blood Pressure tx C-Cigarette Smoking (stop) and Cholesterol (lower) D-Diet and Diabetes E-Education and Exercise

41. CAD: Angina Complications arrhythmias ? myocardial contractility Diagnostic studies thorough history and physical chest X-ray lipid levels cardiac enzymes (isoenzymes), proteins ECG: compare to previous readings PVCs, ventricular tach or fib decrease in contractility results in more ischemia PVCs, ventricular tach or fib decrease in contractility results in more ischemia

42. CAD: Angina Diagnostic studies (continued) treadmill exercise testing 24-hour ECG monitoring nuclear imaging thallium/radioisotope, Dobutamine Stress echo positron emission tomography (PET scan) angiography Exercise testing can show cardiac abnormalities not apparent at rest. As body works, heart must pump harder to supply oxygen. Elevation of ST indicates ischemia Nuclear scans are noninvasive way to tetect presence and significance of coronary artery disease. Pt. given thallium or sestamibi through IV line, then exercise continues. Pt. then scanned in nuclear medicine and again about three hours later to see how much of isotope remains. Areas that are not well perfused show up as �cold� spots. Avoid caffeine 24 hours prior to test. If unable to exercise, can give dobutamine or adenosine IV to increase heart rate and blood pressure, mimicing effects of exercise. Can be used with nuclear or echocardiography. Tilt table to assess cause of syncope (transient loss of consciousness. 24 hour ECG good for Prinzmetal�s Exercise testing can show cardiac abnormalities not apparent at rest. As body works, heart must pump harder to supply oxygen. Elevation of ST indicates ischemia Nuclear scans are noninvasive way to tetect presence and significance of coronary artery disease. Pt. given thallium or sestamibi through IV line, then exercise continues. Pt. then scanned in nuclear medicine and again about three hours later to see how much of isotope remains. Areas that are not well perfused show up as �cold� spots. Avoid caffeine 24 hours prior to test. If unable to exercise, can give dobutamine or adenosine IV to increase heart rate and blood pressure, mimicing effects of exercise. Can be used with nuclear or echocardiography. Tilt table to assess cause of syncope (transient loss of consciousness. 24 hour ECG good for Prinzmetal�s

43. CAD: Angina Diagnostic studies (continued) echocardiography (exercise vs. meds) transesophageal echocardiography (TEE) positron emission tomography (PET) electron beam computed tomography (EBCT) can ID patients with risk factors but no S/S dobutamine to increase heart rate and contractility. Echo uses ultrasound to look at heart. heart chamber size, wall motion, valve movement, structural changes around heart. No info on arteries. TEE good with obesity, emphysema, pt. in atrial fib prior to cardioversion. Left side for TEE, throat sprayed with anesthetic, procedural sedation, need to swallow transducerdobutamine to increase heart rate and contractility. Echo uses ultrasound to look at heart. heart chamber size, wall motion, valve movement, structural changes around heart. No info on arteries. TEE good with obesity, emphysema, pt. in atrial fib prior to cardioversion. Left side for TEE, throat sprayed with anesthetic, procedural sedation, need to swallow transducer

44. CAD: Angina Therapeutic management: Pharmacologic #1 Antiplatelet aggregation therapy ASA 50% reduction in progression USA to MI Antianginals � short and long acting Nitrates dilates peripheral vessels and coronaries ACE inhibitors or ARBs Beta-adrenergic blockers cardioprotective, < morbidity and mortality lessens cardiac workload beta blockers: decrease contractility, HR, SVR, B/P NTG: don�t work if severe disease. should relieve pain in about 3 minutes, lasts up to 45 minutes take up to 3 tabs, 3-5 minutes apart, then 911 dark container, no sunlight new supply q 6-12 months if doesn�t burn under tongue, probably not efficacious spray faster acting transdermal: steady release, sometimes removed to prevent tachyphylaxis. Long-acting: isosorbide dinitrate (Isordil) IV: treatment USA SE? headache, hypotension, check B/P prior to administration.beta blockers: decrease contractility, HR, SVR, B/P NTG: don�t work if severe disease. should relieve pain in about 3 minutes, lasts up to 45 minutes take up to 3 tabs, 3-5 minutes apart, then 911 dark container, no sunlight new supply q 6-12 months if doesn�t burn under tongue, probably not efficacious spray faster acting transdermal: steady release, sometimes removed to prevent tachyphylaxis. Long-acting: isosorbide dinitrate (Isordil) IV: treatment USA SE? headache, hypotension, check B/P prior to administration.

45. Management of Angina Calcium channel blockers Therapeutic Management:Reperfusion Percutaneous coronary intervention (PCI) benefits complications Balloon dilation Stent placement Atherectomy CABG coronary artery bypass grafting diltiazem (Cardizem) lessens angina, B/P systemic vasodilator, decreases contractility, potentiates digoxin so watch for S/S dig toxicity. A common side effect is peripheral edema. PCI: less invasive, shorter recovery, combined with newer drugs? Complications: dissection of artery with rupture cardiac tamponade ischemia/infarction embolus spasm restenosis (30%) in 3-6 months, more in smokers, hyperlipidemia, DM Thrombin inhibitors used in cath lab: bivalrudin (Angiomax) lepirudin (Refludan) orgatroban (Acova) diltiazem (Cardizem) lessens angina, B/P systemic vasodilator, decreases contractility, potentiates digoxin so watch for S/S dig toxicity. A common side effect is peripheral edema. PCI: less invasive, shorter recovery, combined with newer drugs? Complications: dissection of artery with rupture cardiac tamponade ischemia/infarction embolus spasm restenosis (30%) in 3-6 months, more in smokers, hyperlipidemia, DM Thrombin inhibitors used in cath lab: bivalrudin (Angiomax) lepirudin (Refludan) orgatroban (Acova)

46. Collaborative CareAngina Treatment for stable angina: ? oxygen demand and/or ? oxygen supply Nitrate therapy Stent placement Percutaneous coronary intervention Atherectomy Laser angioplasty Myocardial revascularization

47. Collaborative CareAngina Percutaneous coronary intervention Surgical intervention alternative Performed with local anesthesia Ambulatory 24 hours after the procedure Stent placement Used to treat abrupt or threatened abrupt closure and restenosis following PCI

48. Collaborative CareAngina Atherectomy The plaque is shaved off using a type of rotational blade Decreases the incidence of abrupt closure as compared with PCI Laser angioplasty Performed with a catheter containing fibers that carry laser energy Used to precisely dissolve the blockage

49. Collaborative CareAngina Myocardial revascularization (CABG) Primary surgical treatment for CAD Patient with CAD who has failed medical management or has advanced disease is considered a candidate MIDCABG procedure Minimally invasive direct coronary artery bypass grafting (MIDCABG) Alternative to traditional CABG

50. Angina: Nursing Management Assessment history risk factors pain characteristics (PQRST), (OLDCART) Nursing diagnoses pain r/t ischemic myocardium anxiety r/t diagnosis, pain, uncertainty about future decreased cardiac output r/t myocardial ischemia activity intolerance r/t myocardial ischemia P precipitating factors Q quality of pain (dull, sharp) R radiation S severity (pain scale) T timing or when did it begin, any change and have you had before?P precipitating factors Q quality of pain (dull, sharp) R radiation S severity (pain scale) T timing or when did it begin, any change and have you had before?

51. Angina: Nursing Management Planning pain relief decrease anxiety verbalize adequate knowledge of problem, treatment modify risk factors Interventions Emergency treatment chest pain ABCs

52. Angina: Nursing Management Emergency treatment chest pain (MONA) Morphine sulfate if pain unrelieved Oxygen NTG spray, or sublingual or IV if indicated ASA 325mg 2 large gauge IV lines cardiac monitor, 12-lead ECG (gold standard) soon as possible, VS history when able or family present. assess contraindications thrombolytic therapy send to cardiac cath lab within 30 minutes > B/P and HR> B/P and HR

53. Angina: Nursing Management Assessment of pain, response to meds get detail pain characteristics use pain scale Monitor blood pressure, heart tones Chronic management of angina Teach nitroglycerin administration/storage precipitating factors, S/S angina vs. MI personal risk factors diet and exercise Typically may hear gallop or murmur, Angina not life-threatening, give tools to improve QOLTypically may hear gallop or murmur, Angina not life-threatening, give tools to improve QOL

54. Myocardial Infarction (MI) Pathophysiology acute coronary syndrome ischemia irreversible cellular death, necrosis increased mortality first 24 hours 30-50% pre-hospital mortality from lethal arrhythmias. Cell death (cellular contents spill out) ST elevation MI non ST elevation MI many MIs involve left ventricle STEMI and non STEMI treated differently STEMI tx thrombolytics, PCI or other revascularization NSTEMI primarily treated with medicationsSTEMI and non STEMI treated differently STEMI tx thrombolytics, PCI or other revascularization NSTEMI primarily treated with medications

55. Etiology and Pathophysiology Coronary spasm - The constriction is transient and reversible Causes either subtotal or total narrowing Myocardial cyanosis occurs within the 1st 10 seconds of coronary occlusion ECG changes Total occlusion ? anaerobic metabolism and lactic acid accumulation

56. Time is Tissue 4-6 hours without O2 for tissue to die Apoptosis Stunned Myocardium Hibernating Myocardium

57. Etiology and Pathophysiology Myocardial Infarction Occurs as a result of sustained ischemia, causing irreversible cellular death Myocardial Infarction The degree of altered function depends on the area of the heart involved and the size of the infarct

58. Etiology and Pathophysiology Myocardial Infarction Contractile function of the heart stops in the areas of myocardial necrosis Most involve the left ventricle (LV) Types of Myocardial Infarction Transmural MI Involves the entire thickness of the myocardium

59. Etiology and Pathophysiology Myocardial Infarction Subendocardial MI The damage has not penetrated through the entire thickness Infarctions are described by the area of occurrence

60. Etiology and PathophysiologyHealing Process Within 24 hours, leukocytes infiltrate the area of cell death Enzymes are released from the dead cardiac cells (important indicators of MI) Proteolytic enzymes of neutrophils and macrophages remove all necrotic tissue by 2nd or 3rd day Development of collateral circulation improves areas of poor perfusion Necrotic zone identifiable by ECG changes and nuclear scanning 10 to 14 days after MI, scar tissue is still weak

61. Etiology and PathophysiologyHealing Process By 6 weeks after MI, scar tissue has replaced necrotic tissue Area is said to be healed Ventricular remodeling In an attempt to compensate for the infarcted muscle, the normal myocardium will hypertrophy and dilate

63. RCA inferior LAD anterior circumflex lateral, posterior, inferiorRCA inferior LAD anterior circumflex lateral, posterior, inferior

65. ST elevation and inverted T wave. Q wave in several days (4-10)ST elevation and inverted T wave. Q wave in several days (4-10)

66. Clinical Manifestations Myocardial Infarction Pain Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration The hallmark of an MI Nausea and vomiting Can result from reflex stimulation of the vomiting center by the severe pain Sympathetic nervous system stimulation ? catecholamines released during initial phases of MI Results in diaphoresis and vasoconstriction

67. Clinical Manifestations Myocardial Infarction Pain Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration The hallmark of an MI Nausea and vomiting Can result from reflex stimulation of the vomiting center by the severe pain Sympathetic nervous system stimulation ? catecholamines released during initial phases of MI Results in diaphoresis and vasoconstriction

68. Clinical Manifestations Myocardial Infarction Fever May ? within 1st 24 hours up to 100.4� May last as long as 1 week Systemic manifestation of the inflammatory process caused by cell death Cardiovascular manifestations ? BP and heart rate initially Later the BP may drop from ? CO ? urine output Crackles Hepatic engorgement Peripheral edema

69. Myocardial Infarction (MI) Complications post-MI Arrhythmias occur in 80% CHF cardiogenic shock papillary muscle dysfunction ventricular aneurysm pericarditis Dressler syndrome (post-MI syndrome) right ventricular infarction complete heart block, ventricular arrhythmias CHF decrease pump capability: S/S dyspnea, restless, increasein HR, crackles cardiogenic shock: 10-15% mortality papillary muscle: if nearby infarct, systolic murmur aneurysm due to thinwall, bulges out with each contraction pericarditis: 2-4 days post, chest pain worsening with inspiration, diffuse ST elevation Dressler pericarditis with effusion R ventricular infarction; inferior MI, S/S right heart failure; increase fluids, give inotropescomplete heart block, ventricular arrhythmias CHF decrease pump capability: S/S dyspnea, restless, increasein HR, crackles cardiogenic shock: 10-15% mortality papillary muscle: if nearby infarct, systolic murmur aneurysm due to thinwall, bulges out with each contraction pericarditis: 2-4 days post, chest pain worsening with inspiration, diffuse ST elevation Dressler pericarditis with effusion R ventricular infarction; inferior MI, S/S right heart failure; increase fluids, give inotropes

70. Complications of Myocardial Infarction Arrhythmias Most common complication Present in 80% of MI patients Most common cause of death in the prehospital period Congestive heart failure A complication that occurs when the pumping power of the heart has diminished

71. Complications of Myocardial Infarction Cardiogenic shock Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure Requires aggressive management Papillary muscle dysfunction Causes mitral valve regurgitation Condition aggravates an already compromised LV

72. Complications of Myocardial Infarction Ventricular aneurysm Results when the infarcted myocardial wall becomes thinned and bulges out during contraction Pericarditis An inflammation of the visceral and/or parietal pericardium May result in cardiac compression, ? LV filling and emptying, and cardiac failure

73. Complications of Myocardial Infarction Dressler syndrome Characterized by pericarditis with effusion and fever that develops 1 to 4 weeks after MI Pulmonary embolism Source of the thrombus may be the roughened endocardium or leg veins

74. Myocardial Infarction (MI) Complications post-MI (continued) pulmonary embolism Diagnostic studies rapid assessment 12-lead ECG, (ST elevation in at least 2 leads) serial measurement of cardiac markers troponin: very sensitive CK-MB albumin cobalt-binding (ACB) troponin cTnI or cTnT, stays elevate 5-14 days CK-MB returns to normal 2-3 days Which test better for suspected extension or new MI on day 4 after first MI changes in albumin occur with MI myoglobin rises rapidly but is not cardiac specifictroponin cTnI or cTnT, stays elevate 5-14 days CK-MB returns to normal 2-3 days Which test better for suspected extension or new MI on day 4 after first MI changes in albumin occur with MI myoglobin rises rapidly but is not cardiac specific

76. Myocardial Infarction (MI) Therapeutic Management CCU care continuous monitoring for arrhythmias and treatment when they occur morphine sulfate IVP oxygen by nasal cannula 2-4 lpm IV lidocaine or amiodarone VS every 1-2 hours PA catheter, arterial line if LV dysfunction MS decreases anxiety, cardiac workload. Watch for resp. depression with first dose.MS decreases anxiety, cardiac workload. Watch for resp. depression with first dose.

77. Therapeutic Management MI Therapeutic Management CCU care anti-platelet aggregation tx. (start in ER or cath lab) decrease incidence of new MI, death, refractory ischemia tirofiban (Aggrastat) intravenous abciximab (Reopro) intravenous eptifibatide (Integrilin) give with aspirin, heparin, lovenox concurrently thrombolytic therapy (start in ER or cath lab) contraindications? What type of drugs? glycoprotein IIB/IIIA Thrombolytics can be given IV or into coronary arteries in cath lab. INDICATIONS: chest pain < 6 hours elevation ST segment 2 or more leads age (riskier if > 65) Do all labs, invasive testing before starting. Need 3 IV lines Monitor ECG for ST segment, reperfusion arrhythmias (have amiodarone and atropine nearby) Monitor CK-MB levels. Biggest risk: bleeding. Watch IV sites, gums. If LOC suddenly changes or blood in NG or stool? TURN OFF!! Contraindications: hx hemorrhagic stroke, uncontrolled HTN (180/120), recent surgery or trauma in last 2 weeks, active internal bleeding, known bleeding disorder, suspected aortic dissection, pregnancy. What type of drugs? glycoprotein IIB/IIIA Thrombolytics can be given IV or into coronary arteries in cath lab. INDICATIONS: chest pain < 6 hours elevation ST segment 2 or more leads age (riskier if > 65) Do all labs, invasive testing before starting. Need 3 IV lines Monitor ECG for ST segment, reperfusion arrhythmias (have amiodarone and atropine nearby) Monitor CK-MB levels. Biggest risk: bleeding. Watch IV sites, gums. If LOC suddenly changes or blood in NG or stool? TURN OFF!! Contraindications: hx hemorrhagic stroke, uncontrolled HTN (180/120), recent surgery or trauma in last 2 weeks, active internal bleeding, known bleeding disorder, suspected aortic dissection, pregnancy.

78. Therapeutic Management MI Other pharmacologic management IV nitroglycerin, antiarrhythmics positive inotropic agents beta-adrenergic blockers calcium-channel blockers angiotensin-converting enzyme inhibitors stool softeners Nutritional management Goals: decrease preload/afterload, increased MVO2. atropine, amiodarone or lidocaine for arrhythmias Inotropes: increase contractility good in LV dysfunction, digoxin, dobutamine, amrinone (Inocor) Beta adrenergic blockers decrease morbidity after MI calcium channel blockers: no statistical evidence of decrese in morbidity/mortality ACE: post AMI help keep heart size small, may slow onset CHF Stool softeners such as Colace to prevent straining (MS, inactivity) STEMI- reperfusion is the goal, thrombolytics, cath lab for PCI NSTEMI- treat with medicationsGoals: decrease preload/afterload, increased MVO2. atropine, amiodarone or lidocaine for arrhythmias Inotropes: increase contractility good in LV dysfunction, digoxin, dobutamine, amrinone (Inocor) Beta adrenergic blockers decrease morbidity after MI calcium channel blockers: no statistical evidence of decrese in morbidity/mortality ACE: post AMI help keep heart size small, may slow onset CHF Stool softeners such as Colace to prevent straining (MS, inactivity) STEMI- reperfusion is the goal, thrombolytics, cath lab for PCI NSTEMI- treat with medications

79. Therapeutic Management MI Nursing Management Assessment thorough history physical, test results Nursing diagnosis Acute pain r/t lactic acid production and altered MVO2 Altered cardiac tissue perfusion r/t myocardial damage, decreased cardiac output Anxiety related to pain, perceived threat of death same as for anginasame as for angina

80. Therapeutic Management MI Nursing Management (continued) Impaired gas exchange r/t ineffective breathing,, decreased systemic tissue perfusion Activity intolerance r/t fatigue d/t decreased cardiac output, poor tissue perfusion Self-esteem disturbance r/t lack of control, illness, and perceived role changes Constipation r/t immobility, change in diet, fluid restriction, meds

81. Therapeutic Management MI Nursing Management (continued) Ineffective management of therapeutic regimen r/t lack of knowledge. Grieving r/t actual or perceived losses secondary to cardiac condition Planning relief of pain no progression of MI receive immediate, correct treatment effective coping with anxiety

82. Therapeutic Management MI Nursing Management (continued) Planning compliance with rehabilitation plan alteration of high-risk behaviors Interventions Reduce myocardial oxygen demand Pain: MS, pain scales, nonverbal signs, NTG titration Monitoring ECG in CCU, telemetry; tx. arrhythmias ventricular fibrillation most lethal

83. Therapeutic Management MI Nursing Management (continued) Interventions Monitoring VS, I and O assessment heart and lung sounds oxygenation, fluid retention, thrombosis Rest/comfort bedrest if severe, gradual increase in activity Anxiety management teaching only if ready, do not force.

84. Therapeutic Management MI Chronic/Home management Cardiac rehabilitation Patient education S/S MI vs. angina identification/reduction of modifiable risk factors Physical exercise Resumption sexual activity 1-2 flights stairs without symptoms Sex: can take NTG prophylactically. No Viagra! Not after heavy meal, excess ETOH increased risk with unfamiliar partners Anal intercourse is risky, oral is OK.Sex: can take NTG prophylactically. No Viagra! Not after heavy meal, excess ETOH increased risk with unfamiliar partners Anal intercourse is risky, oral is OK.

85. Sudden Cardiac Death Pg 817 Unexpected cardiopulmonary arrest Within minutes to one hour after symptoms 350,000 yearly Poor prognosis, only 10% discharged from hospital Multi-vessel coronary arteriosclerosis common Often no previous history Death due to arrhythmias (ventricular tachycardia and or ventricular fibrillation) Risk factors same as for CAD and Ejection fraction < 40% History of ventricular arrhythmias Only 44% of those discharged from hospital will be alive 6 years later. Most have NOT had MI. Risk factors for sudden cardiac death Male Family hx premature atherosclerosis Cigarette smoking Diabetes mellitus Hypercholesterolemia Hypertension Cardiomegaly And EF < 40%, hx. VT, VFOnly 44% of those discharged from hospital will be alive 6 years later. Most have NOT had MI. Risk factors for sudden cardiac death Male Family hx premature atherosclerosis Cigarette smoking Diabetes mellitus Hypercholesterolemia Hypertension Cardiomegaly And EF < 40%, hx. VT, VF

86. Sudden Cardiac Death Therapeutic management Did they have acute MI? Typical MI workup: enzymes, troponin, ECG Cardiac cath to assess degree of problem PTCA vs. CABG Electrophysiology study Possible insertion AICD/ICD Counseling for patient/family Patient/Family education Most have multivessel disease. Fear is common. Must educate!Most have multivessel disease. Fear is common. Must educate!

87. Gerontologic considerations CAD Physiologic changes occur with aging Increased collagen, fat deposition Myofibrillar degeneration Endocardial thickening Calcification of heart valves Degeneration conduction system Loss of elasticity of arteries, > SBP, SVR Decrease in CO 1% per year Increase norepinephrine, slowed response receptors More pacemakers placed in those > 65 years Increase in systolic BP Decrease in CO is d/t decrease contractility, increase in afterload.More pacemakers placed in those > 65 years Increase in systolic BP Decrease in CO is d/t decrease contractility, increase in afterload.

88. Gerontologic considerations CAD Considerations Changes in vital signs occur more slowly Atypical symptoms with acute MI Longer warm-up and cool down periods Watch for heat intolerance, decrease in sweating Increase in unstable angina, CHF, complication related to AMI (arrhythmias!) Watch for early signs/symptoms Treat aggressively Target heart rate 60-75% for older adults Diaphoresis not typical. Sudden onset of dyspnea, fatigue, profound weakness. Beta blockers often of benefit but side effects of CHF and heart block occur more frequently. PTCA of benefit. Elective CABG also well-tolerated but CVA, arrhythmia, infection more common. Polypharmacy.Target heart rate 60-75% for older adults Diaphoresis not typical. Sudden onset of dyspnea, fatigue, profound weakness. Beta blockers often of benefit but side effects of CHF and heart block occur more frequently. PTCA of benefit. Elective CABG also well-tolerated but CVA, arrhythmia, infection more common. Polypharmacy.

89. Women and CAD Myocardial infarction #1 killer women CAD symptoms begin about 10 years later than men Protective female hormones Women have higher mortality/morbidity with fewer returning to work Post-MI, post-CABG Risk factors: diabetes mellitus more influential Smoking is major risk for women in their 40s Hypertension also of major concern When we think of MI, we think of middle-aged men, but� Smoking is thought to lower estrogen levels. Estrogen replacement: linked with no decrease in cardiac risk, increased risk for breast cancer and other diseases. When we think of MI, we think of middle-aged men, but� Smoking is thought to lower estrogen levels. Estrogen replacement: linked with no decrease in cardiac risk, increased risk for breast cancer and other diseases.

90. Women and CAD Typical tests diagnostic for men are not useful in women Exercise stress tests not indicative for women Thallium treadmill much more sensitive Still not as reliable as EST for men Echocardiogram with exercise even better EDUCATE!! Careful assessment when risk factors present (Smoking and Oral contraceptives use) Need to carefully assess women presenting with any pain, do not dismiss. Cardiac rehab has been very good for women. Need to be aware that housework is exercise!Need to carefully assess women presenting with any pain, do not dismiss. Cardiac rehab has been very good for women. Need to be aware that housework is exercise!

91. CAD Review Stable angina Pain characteristics, diagnosis, treatment? Unstable Angina Pain characteristic, diagnosis, treatment? Myocardial Infarction Pain characteristic, diagnosis, treatment? Drug Review BB, Morphine, Nitroglycerin, antilipemics, ASA, lidocaine, amiodarone, thrombolytics

93. CABGCoronary Artery Bypass Graft Surgery Native vessels Saphenous vein Internal mammary artery Off�pump CABG Transmyocardial laser revascularization