Nursing care of client with Coronary Artery Disease Part 1 of 2

NURSING CARE OF CLIENTWITH ACUTE CORONARYSYNDROME

ASSESSMENT, DX EXAMS

Maria Carmela L. Domocmat, RN, MSN InstructorSchool of Nursing Northern Luzon Adventist College

CORONARY ARTERY DISEASE

CLDomocmat 8/9/2012 2

Coronary Artery Disease

AKA

� Ischemic Heart Disease

� Coronary Heart Disease (CHD)

� Coronary Occlusive Disease (C.O.D.)

� Atherosclerotic Heart Disease (A.H.D.)


Coronary Artery DiseaseCoronary Artery Disease

�� Refers to the diseases of the heart that Refers to the diseases of the heart that result from a decrease in blood supply to result from a decrease in blood supply to the heart muscle the heart muscle

�� Disease caused by inadequate supply of Disease caused by inadequate supply of �� Disease caused by inadequate supply of Disease caused by inadequate supply of blood to the heart.blood to the heart.


CAD

� Include the disorders

1. Angina pectoris

2. Acute coronary syndrome 2. Acute coronary syndrome

a. Unstable angina

b. MI (STEMI, NSTEMI)

8/9/2012CLDomocmat 5

�� IncidenceIncidence

�� Primary cause of morbidity mortality in the Primary cause of morbidity mortality in the PhilippinesPhilippines

�� EtiologyEtiology

�� Results from development of Results from development of obliterativeobliterativelesions within the coronary arterieslesions within the coronary arteries


Ten Leading Causes of MortalityPhilippines, 20001. Diseases of the Heart

2. Diseases of the Vascular System

3. Malignant Neoplasm

4. Pneumonia

5. Accidents5. Accidents

6. Tuberculosis, all forms

7. Chronic Obstructive Pulmonary Disease & Allied Conditions

8. Certain conditions originating in the Perinatal period

9. Diabetes Mellitus

10. Nephritis, Nephrotic Syndrome and Nephrosis

8/9/2012CLDomocmat 7http://www.doh.gov.ph/files/table1_4.pdf

Coronary Artery Disease

� Occlusion of the coronary artery or any of its branches

� Decrease or absence of blood supply to myocardium

1. Transient Hypoxia:

Angina Pectoris

2. Hypoxia with decreased function: Myocardial Ischemia

3. Death and necrosis of myocardium: Myocardial Infarction



Causes of CAD

�� ArteriosclerosisArteriosclerosis�� AtherosclerosisAtherosclerosis


AtherosclerosisAtherosclerosis –– deposition of fat deposition of fat

containing substances along the containing substances along the intimaintima of of blood vessels causing its narrowing ; a type blood vessels causing its narrowing ; a type of arteriosclerosisof arteriosclerosisof arteriosclerosisof arteriosclerosis


atherosclerosis



Atheroma Formation



� Atherosclerosis develops in the coronary arteries, causing them to become narrowed or blocked. Blood flow to the area of the heart supplied area of the heart supplied


ArteriosclerosisArteriosclerosis

�� Is hardening of Is hardening of arteriearterie

�� primarily affects the primarily affects the intimalintimal layer of the blood vesselslayer of the blood vessels

�� Includes: Includes:

�� a. Atherosclerosisa. Atherosclerosis –– accumulation of fat accumulation of fat �� a. Atherosclerosisa. Atherosclerosis –– accumulation of fat accumulation of fat depositsdeposits

�� b. b. MonckebergsMonckebergs sclerosissclerosis –– calcium calcium accumulation in medial layers of the accumulation in medial layers of the arteriesarteries

�� c. Arteriolar sclerosisc. Arteriolar sclerosis-- thickening of the thickening of the small artery vesselssmall artery vessels

��



Theories of PathogenesisTheories of Pathogenesis

1.1. Response to injury theoryResponse to injury theory

2.2. NeoplasiaNeoplasia TheoryTheory


Theories of PathogenesisTheories of Pathogenesis

1. Response to injury theory1. Response to injury theoryInjurious Stimuli (HPN, Hypercholesterolemia)Injurious Stimuli (HPN, Hypercholesterolemia)

Endothelial damageEndothelial damage

Increased permeability/adhesion moleculeIncreased permeability/adhesion molecule

Lipids and platelets travel to the areas affectedLipids and platelets travel to the areas affected


Migration of macrophages into vessel wallMigration of macrophages into vessel wall

Plaques begin to form from cells which are imbibed Plaques begin to form from cells which are imbibed

into the endotheliuminto the endothelium

Lipids are engulfed by the cells (foam cells) and Lipids are engulfed by the cells (foam cells) and

smooth muscle cells developsmooth muscle cells developsmooth muscle cells developsmooth muscle cells develop

Narrowing of blood vesselsNarrowing of blood vessels

Plaque disruptionPlaque disruption


Thrombus formationThrombus formation

Obstruction of coronary arteriesObstruction of coronary arteries

Decreased Myocardial OxygenationDecreased Myocardial Oxygenation

Angina pectorisAngina pectoris

Myocardial InfarctionMyocardial Infarction


2. 2. NeoplasiaNeoplasia TheoryTheory

-- vessel injury cause cell proliferation vessel injury cause cell proliferation stemming from a single cell (monoclonal stemming from a single cell (monoclonal origin)origin)stemming from a single cell (monoclonal stemming from a single cell (monoclonal origin)origin)


Aortic atherosclerotic plaques Aortic atherosclerotic plaques


Cross section of a coronary artery. A thrombus occludes the Cross section of a coronary artery. A thrombus occludes the

lumen and rests upon a mature atherosclerotic plaque. Note lumen and rests upon a mature atherosclerotic plaque. Note

the relative thickness of the intima and media. the relative thickness of the intima and media.


�Nonmodifiable risk factors�Modifiable risk factors

Etiology and risk factors


Nonmodifiable risk factors

� Heredity

� Increasing age

� Gender


Heredity

� family history of first degree relative with CVD at 55 yrs old or younger (M), 65 yrs old or younger (F)


Increasing age

� ›45 yrs old (M); ›55 yrs old (F)


GenderGender

�� affects men more than women before affects men more than women before they have menopausethey have menopause

�� with OCP use after menopause increase with OCP use after menopause increase risk of developing CAD especially with risk of developing CAD especially with smoking historysmoking historyrisk of developing CAD especially with risk of developing CAD especially with smoking historysmoking history

�� with early menopausewith early menopause-- 3x’s increase risk 3x’s increase risk of developing CADof developing CAD

�� lifestyle changes that increase risk of CAD lifestyle changes that increase risk of CAD in womenin women�� a. more women have entered the work forcea. more women have entered the work force�� b. increase number of smokersb. increase number of smokers


Modifiable risk factors

� Cigarette smoking

� Hypertension

� Increase serum cholesterol

� Homocysteine levels

� Metabolic syndrome

� Physical inactivity cholesterol

� Lack of exercise

� Obesity

� Diabetes

� Stress

� Inflammatory Response


Cigarette smokingCigarette smoking

� Nicotine – initiate release of catecholamine

� Endothelial dysfunction and increased vessel wall thickness vessel wall thickness

� Increase blood CO level

� Beware! Passive smoking

� Oral contraceptives (OC) + smoking


HypertensionHypertension

� men >45 y/o with BP exceeding 140/90

� all adult women with pressures above 160/95 have a 50% increase in mortalitymortality

� the higher the BP = the higher the risk of CAD


Increase serum cholesterolIncrease serum cholesterol

� > 259mg/dl = 3x’s more likely to develop CAD

�� Patients with LDL to HDL ratios greater than Patients with LDL to HDL ratios greater than 4:1 are prone to CAD4:1 are prone to CAD4:1 are prone to CAD4:1 are prone to CAD


Modifiable Risk Factors Modifiable Risk Factors cont.cont.

�� Lack of exerciseLack of exercise

�� Obesity Obesity

� Distribution of body fat

� Waist measurement: N: less than 40 inches (M); � Waist measurement: N: less than 40 inches (M); less than 35 (F)

� BMI – N: 18.5 to 24.9

�� DiabetesDiabetes

�� Stress: Stress: increases BPincreases BP


Metabolic syndrome Metabolic syndrome

� Diagnosis of this includes 3 of the ff:� Insulin resistance (FBS › 100 mg/dl or

abnormal GTT)

� Central obesity (waist circum › 35 inches for F; � Central obesity (waist circum › 35 inches for F; › 40 for M

� Dyslipedemia (Tg ›150 mg/dL; HDL ‹ 50 mg/dL for F; ‹ 40 mg/dL for M)

� BP persistent ›130/85

� Proinflammatory state (high CRP level)

� Prothtombin state (high fibrinogen level)


Inflammatory responses

� chronic inflammation cause increase C-reactive protein (CRP) levels which tend to disrupt plaque inside arterial walls

Lab test : high sensitivity C-reactive � Lab test : high sensitivity C-reactive protein (hs-CRP)


Homocystein levels

� Essential amino acid

� High serum levels block production of

� High homocysteinelevels increase the risks of a heart attack or stroke.

block production of nitric oxide

� Normal value: ‹ 12 mmol/dL

attack or stroke.


Physical inactivity

� Goal: 30 minutes, regular moderate aerobic exercise (ex: brisk walking)


Let’s Review


Modifiable risk factors

� Cigarette smoking

� Hypertension

� Increase serum cholesterol

� Homocysteine levels

� Metabolic syndrome

� Physical inactivity cholesterol

� Lack of exercise

� Obesity

� Diabetes

� Stress

� Inflammatory Response


Prevention


An ounce of prevention is better

than a pound of curethan a pound of cure


Preventive measures

�� Lifestyle modificationsLifestyle modifications

�� Reduce stressReduce stress

�� BP control, DM controlBP control, DM control�� BP control, DM controlBP control, DM control

� Lower Serum chole

� Reduce CRP levels ((hshs--CRP)CRP)

� Lower Homocystein levelsBoost “good cholesterol” levels (HDL)Boost “good cholesterol” levels (HDL)


Lifestyle modificationsLifestyle modifications

�� Diet: low fat , low cholesterol, low saltDiet: low fat , low cholesterol, low salt

�� quit smoking , avoid passive smokingquit smoking , avoid passive smoking

�� exercise and weight reductionexercise and weight reduction�� exercise and weight reductionexercise and weight reduction

�� adequate time for rest and relaxationadequate time for rest and relaxation


MedicationsMedications

�� statinsstatins

�� Glycoprotein Glycoprotein IIbIIb//IIIaIIIa receptor receptor antagonistsantagonists

�� aspirin, aspirin, plavixplavix� Aspirin in low doses is the best known agent

for the prevention of coronary heart disease.


Cigarette smoking cessationCigarette smoking cessation

� Educational program, Counseling, Consistent motivation, reinforcement messages, support group,

meds � meds

� nicotine patch [NicoDerm CQ, Habitrol]

� antidepressant bupropim [Zyban])


Exercise and weight reductionExercise and weight reduction

� Goal: 30 minutes, regular moderate aerobic exercise (ex: brisk walking)

� EBP:

� Men who had weights 30 min or more per week had a 23% risk reduction in coronary heart disease


Reduce Serum chole

� Serum fasting lipid profile at least q 5 yrs

� Lipid-lowering meds� Statins

� Nicotinic acid

� Fibric Acids

� Bile acid sequestrants

� Cholesterol absorption inhibitor

� Omega-3-acid-ethyl esters


Statins

� block a substance liver needs to make cholesterol.

� This reduces cholesterol in liver cells, which � This reduces cholesterol in liver cells, which causes liver to remove cholesterol from your blood.

� may also help body reabsorb cholesterol from built up deposits on your artery walls.


http://www.mayoclinic.com/health/hdl-cholesterol/CL00030/NSECTIONGROUP=2

Statins

� atorvastatin (Lipitor)

� fluvastatin (Lescol)

� lovastatin (Altoprev, Mevacor)

� pravastatin (Pravachol)� pravastatin (Pravachol)

� rosuvastatin (Crestor)

� simvastatin (Zocor)



EBP: Statins

� Statin Drugs and Dietary Supplements – Vit. E and C, selenium plus statin resulted into reduced LDL levels compared to statinsalone.alone.


Reduce CRP levels ((hshs--CRP)CRP)

� Low fat, low chole diet

� Smoking cessation

� Exercise

� Statin

� Aspirin


Lower Homocystein levels

� B-complex vitamin (esp folic acid)


Boost your “good cholesterol” Boost your “good cholesterol” levels (HDL): levels (HDL): Set your target HDL cholesterol level

At risk Desirable

Less than 40 60 mg/dL (1.6

Men

Less than 40

mg/dL (1.0

mmol/L)

60 mg/dL (1.6

mmol/L) or above

Women

Less than 50

mg/dL (1.3

mmol/L)

60 mg/dL (1.6

mmol/L) or above


http://www.mayoclinic.com/health/hdl-cholesterol/CL00030

Boost your “good cholesterol” Boost your “good cholesterol” levels (HDL)levels (HDL)� Don't smoke.

� Lose weight

� Get more physical activity.

� Drink alcohol only in moderation

� Choose healthier fats.

� Monounsaturated and polyunsaturated fats —found in olive, peanut and canola oils

� Nuts, fish and other foods containing omega-3 fatty acids



EBP: Alcohol

� Compared with men who consume alcohol less than once a week, men who consume alcohol 3-7 days a week had a 32%-37% reduction of MI. had a 32%-37% reduction of MI.


Boost your “good cholesterol”Boost your “good cholesterol”

� Choose healthier fats.

� Monounsaturated and polyunsaturated fats —found in olive, peanut and canola oils

� Nuts, fish and other foods containing omega-3 � Nuts, fish and other foods containing omega-3 fatty acids



Boost your “good cholesterol”Boost your “good cholesterol”

� Niacin (Niaspan)

� Fibrates

� The medications fenofibrate (Lofibra, Tricor) and gemfibrozil (Lopid) can also help increase and gemfibrozil (Lopid) can also help increase HDL cholesterol level.



See separate presentation

Stable and Unstable Angina PectorisStable and Unstable Angina Pectoris


Acute Myocardial InfarctionAcute Myocardial Infarction


Acute Myocardial InfarctionAcute Myocardial Infarction

�� Occurs when myocardial tissue is abruptly Occurs when myocardial tissue is abruptly and severely deprived of O2and severely deprived of O2

�� When blood flow is reduced by 80When blood flow is reduced by 80--90% 90% ischemia developsischemia developsischemia developsischemia develops


�� prolonged ischemia lasting more than 35prolonged ischemia lasting more than 35--45 minutes produces irreversible cellular 45 minutes produces irreversible cellular damage damage and necrosis of the and necrosis of the myocardium myocardium myocardium myocardium

�� ischemic injury evolves over several hours ischemic injury evolves over several hours toward complete necrosis and infarctiontoward complete necrosis and infarction


� The autonomic nervous system attempts to compensate for the depressed cardiac performance.

� This results to further imbalance between � This results to further imbalance between myocardial oxygen supply and demand

� The 3 areas which develop in MI are:


CLDomocmat

http://pathologyproject.files.wordpress.com/2011/03/early-signs.jpg

8/9/2012 65

Zone of infarctionZone of infarction

Zone of hypoxic injury

Zone of ischemiaZone of ischemia


Most common site for MI is the anterior wall of the left ventricle.

� MI may be classified as follows:� Transmural infarct – extends from endocardium

to epicardium

� Subendocardial – affects the endocardial muscles

� Intramural – seen in patchy areas of the � Intramural – seen in patchy areas of the myocardium and is usually associated with longstanding angina pectoris

� Healing requires formation of scar tissues that replace the necrotic myocardium; scar tissue inhibits contractility



javascript:eml2('dorland','infarction_myocardial.jpg')


Clinical ManifestationsClinical Manifestations



�� Pain Pain �� crushing, severe, prolonged, unrelieved by crushing, severe, prolonged, unrelieved by

rest or nitroglycerine, radiating to one or rest or nitroglycerine, radiating to one or both arms, neck, backboth arms, neck, backboth arms, neck, backboth arms, neck, back

�� Signs of shockSigns of shock -- hypotension, cold hypotension, cold diaphoresis, peripheral cyanosis, diaphoresis, peripheral cyanosis, tachytachy//bradybrady, , threadythready pulsepulse


� Women often present with a “triad” of symptoms, including indigestion or abdominal fullness, chronic fatigue despite adequate rest, and inability to catch one’s adequate rest, and inability to catch one’s breath.



� fever� apprehension� indigestion� dob� dob� n/v� pallor, cyanosis, coolness of extremities� increase BP, HR, S4, transient murmur


PE

� thorough and focused health hx and PE

� goal: presence of CAD risk factors, angina, previous infarctions

� focused assessment � focused assessment � chest pain

� general appearance

� determination of frequent VS

� cont monitoring of cardiac and pulse

� ongoing eval of mental status, heart, lungs, abd UO, extremities

8/9/2012Maria Carmela L.Domocmat, RN, MSN 75

Diagnostic exams


Diagnostic exams

� ECG

� Serum Markers of Myocardial Damage : Cardiac biomarkers

� Cardiac catheterization with coronary arteriographyarteriography

� Echocardiography

� Radionuclide imaging

� PET Scan

� CT scan

� Magnetic Resonance Imaging

� Intravascular ultrasound (IVUS)



Stress ECGStress ECG

�� ST segment ST segment depression of 1mm or depression of 1mm or more during exercise more during exercise

�� ECG changes during ECG changes during �� ECG changes during ECG changes during testing may indicate testing may indicate

ischemiaischemia


12 lead ECG changes12 lead ECG changes

�� T wave inversionT wave inversion

�� ST segment elevation (ST segment elevation (subepicardialsubepicardialinjury)injury)

�� ST segment depression ST segment depression ((subendocardialsubendocardial injury)injury)

�� abnormal Q wave (infarction)abnormal Q wave (infarction)





http://www.technion.ac.il/~eilamp/mi_qwave.html

Abnormal Q wave


12- lead ECG

� Note: 1 single ECG is NOT sufficient to confirm or exclude dx of AMI

� cardiac conduction system is dynamic process that is subject to change overtime that is subject to change overtime

� Recommendation

� serial ECGs q 30 min for pt at high risk for AMI


Acute Cardiac Ischemia Time-Insensitive Predictive Instrument (ACI-TIPI)

Adobe Acrobat Adobe Acrobat


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Serum Markers of Myocardial Serum Markers of Myocardial Damage : Damage : Cardiac biomarkers


Cardiac Serum markers

� during infarction process – cell membranes rupture, allowing intracellenzymes to spill out into blood stream

� are substances that are released into the blood when the heart is damaged or

� are substances that are released into the blood when the heart is damaged or stressed.

� Measurement of these biomarkers is used to help diagnose, risk stratify, monitor and manage people with suspected acute coronary syndrome (ACS) and cardiac ischemia.


Cardiac biomarkers

� Current cardiac biomarker tests used to help diagnose, evaluate, and monitor individuals suspected of having acute coronary syndrome (ACS) include:coronary syndrome (ACS) include:

� Troponin I or T

� CK-MB


Cardiac biomarkers

� Other biomarker tests that may be used:� Myoglobin� BNP (or NT-proBNP) — although usually used to recognize

heart failure, an increased level in people with ACS indicates an increased risk of recurrent events

� hs-CRP� hs-CRP� Homocysteine

� Phased out biomarkers—the tests below are not specific for damage to the heart and are no longer recommended for evaluating people with suspected ACS:� AST� LDH


Cardiac Troponin T and I

� most sensitive to cardiac muscle damage

� Not found in normal heart

� quick, rapid test

� if elevated – indicate AMI

� become elevated in the blood within 3 or 4 hours after injury and may remain elevated for 10 to 14 days.


Troponin

� Troponin T

� similar to CK-MB – with regard sensitivity

� useful and more accurate than LDH in confirmation of distant AMI confirmation of distant AMI

� Troponin I

� very specific and sensitive indicator of AMI

� not affected by any other dse or injury to any other muscle except cardiac muscle


CK MB

� Enzyme specific to cells of heart

� (+) in blood indicates tissue necoris or injury


MyoglobinMyoglobin

�� found in both skeletal and cardiac found in both skeletal and cardiac musclemuscle

�� Detected 2Detected 2--3 hours post MI3 hours post MI�� Detected 2Detected 2--3 hours post MI3 hours post MI


Myoglobin

� start to rise within 2-3 hours of a heart attack or other muscle injury, reach their highest levels within 8-12 hours, and generally fall back to normal within one day.

Increase is detectable sooner than troponin, � Increase is detectable sooner than troponin, but it is not as specific for heart damage and it will not stay elevated as long as troponin.

� Although a negative myoglobin result effectively rules out a heart attack, a positive result must be confirmed by testing for troponin.

8/9/2012CLDomocmat 96http://labtestsonline.org/understanding/analytes/myoglobin/tab/test

TestTest Time to Time to

detectiondetection

Peak Peak DurationDuration SamplingSampling

CKCK--MBMB 66--12 hours12 hours 1 day1 day 3 days3 days Every 12 hrs x 3 Every 12 hrs x 3

days start 6 hrs days start 6 hrs

after chest painafter chest pain

TroponinTroponin TT 33--12 hours12 hours 24 hours24 hours 1010--14 days14 days One at least 12 hrs One at least 12 hrs

after onset of painafter onset of pain

TroponinTroponin II 33--12 hours12 hours 24 hours24 hours 55--10 days10 days One at least 12 hrs One at least 12 hrs

after onset of painafter onset of pain

MyoglobinMyoglobin 11--3 hrs3 hrs 12 hrs12 hrs


Lactate dehydrogenase (LDH or LD) � is an enzyme that is found in almost all of

the body's cells, but only a small amount of it is usually detectable in the blood.

� is released from the cells into the � is released from the cells into the bloodstream when cells are damaged or destroyed. Because of this, the LDH test can be used as a general marker of injury to cells.


http://labtestsonline.org/understanding/analytes/ldh/tab/test

LDH

� LDH1 subunit – plentiful in heart muscle and released into serum when myocardial damage occurs

� LDH-1: heart, red cells, kidney, germ cells� LDH-1: heart, red cells, kidney, germ cells

� LDH-2: heart, red blood cells, kidney (lesser amounts than LDH-1)

� LDH-3: lungs and other tissues

� LDH-4: white blood cells, lymph nodes, muscle, liver (lesser amounts than LDH-5)

� LDH-5: liver, skeletal muscle


Nrg considerations: LDH

� Inform that no need to restrict food or fluids

� Muscle trauma caused by MI injections can raise LD levelscan raise LD levels

� Prosthetic valves or recent surgery or pregnancy can cause elevated result


TestTest Time to Time to

detectiondetection

Peak Peak DurationDuration SamplingSampling

SGOTSGOT 24 hours24 hours 2 days2 days 4 days4 days 11--2 days 2 days

after chest after chest

painpain


painpain

LDHLDH 36 hours36 hours 3 days3 days 10 days10 days 11--2 days 2 days

after chest after chest

painpain

Other lab tests

� Serum lipids

� Hs CRP

� Homocystein

� WBC

� Serum elec


Fasting lipid profile

� total cholesterol: ‹ 200 mg/dL

� triglycerides : ‹ 150 mg/dL

� LDL : ‹ 100 mg/dL

� HDL chole: ‹ 60 mg/dL

� HDL: LDL ratio shld be 3:1


Homocystein levels

� Normal value: ‹ 12 mmol/dL

� Labs: NPO 1-12 hrs


High sensitive CHigh sensitive C-- reactive protein reactive protein ((hshs--CRP)CRP)

�� correlates with CKcorrelates with CK--MB levels but it MB levels but it peaks several days laterpeaks several days later

�� Most standard marker of inflammationMost standard marker of inflammation�� Most standard marker of inflammationMost standard marker of inflammation

�� Normal value: 1 mg/dlNormal value: 1 mg/dl

� > 3 – increase risk CAD


Leukocytosis

� 10, 000 to 20, 000 mm3

� appears on 2nd day

� disappears in 1 wk

� Myeloperoxidase – a leukocyte enzyme –recently shown to ne a predictive ofAMIeven in clients without elevation in Troponin T


Cardiac catheterization with coronary arteriography


Cardiac catheterization with coronary arteriography�� direct visualization of direct visualization of

the coronary arteries the coronary arteries by selective injection by selective injection of radiographic of radiographic of radiographic of radiographic contrast materialcontrast material

�� most sensitivemost sensitive and and specific specific testtest


Cardiac catheterization with coronary arteriographypre post

� Determine allergy to iodine and seafoods (prep antihistamine)

� Bed rest� Supine HOB elevate� Leg insertion site keep

straight� Informed consent

� 2-6 hrs bedrest

� NPO post MN

� VS, auscultate heart and lungs, eval peripheral pulses, withheld digitalis or diuretics

�

straight

� VS q 15v min for 1 hr; then q 30 for 2 hrs til stable

� Analgesics

� Assess insertion site

� VS, auscultate heart and lungs, eval peripheral pulses,

� Observe complication


Health educ post cath

� For the next 24 hrs

� Don’t bend at waist

� Strain

� Lift heavy objects � Lift heavy objects

� Avid tub bath

� Call doctor if

� Bleeding, swelling, new bruising from peripheral site, temp >38.6C


Cardiac catheterization



Coronary angiography

� Let’s watch

http://video.about.com/heartdisease/Angiography.htm


YouTube - Heart Animation_ Coronary Angiography _Cardiac Catheterization_.flv

EchocardiographyEchocardiography


EchocardiographyEchocardiography -- produces images of wall produces images of wall motion abnormalitiesmotion abnormalities


Transesophageal Transesophageal EchocardiographyEchocardiography


Radionuclide imagingRadionuclide imaging


Radionuclide imagingRadionuclide imaging

�� Stress Stress scintigraphyscintigraphy -- use of thallium use of thallium 201 or 201 or sestamibisestamibi

�� --decrease uptake of dye in ischemic tissuedecrease uptake of dye in ischemic tissue

�� Stress radionuclide Stress radionuclide ventriculographyventriculography�� Stress radionuclide Stress radionuclide ventriculographyventriculography-- pyrophosphate injected peripherally pyrophosphate injected peripherally binds the radionuclide technetium to RBCbinds the radionuclide technetium to RBC

�� used to produce a used to produce a scintigraphicscintigraphic image of image of the left ventriclethe left ventricle

�� 90% sensitive90% sensitive


PET ScanPET Scan


PET ScanPET Scan


PET ScanPET Scan

� 3 dimensional images

� Inject isotopes

� Avoid tobacco and caffeine 4 hrs before


CT scan


CT scan

� Xray

� Cross sectionial images of the chest (heart, great vessels)

Evaluate cardiac masses and dse of aorta � Evaluate cardiac masses and dse of aorta , pericardium


Magnetic Resonance ImagingMagnetic Resonance ImagingMagnetic resonance angiographyMagnetic resonance angiography


Magnetic Magnetic Resonance ImagingResonance Imaging


Magnetic Resonance ImagingMagnetic Resonance Imaging

� No metal can enter the exam room� clothing with metal snaps or pins should not be

worn. � Jewelry, watches, rings etc should be left in a

locker. locker. � Hairpins and dentures, should also be removed

and left in a locker or outside the exam room � Heavy facial makeup should not be worn as it may

create artifacts on the image.

� Labs are not required unless have a history of impaired kidney function. However, allergy history records are necessary for contrast studies.


Magnetic Resonance ImagingMagnetic Resonance Imaging

� Contraindication� Patients cannot have halter monitors, telemetry units,

nerve stimulation units or a IV pump in the magnet room

� If have a heart pacemaker or pacing wires, cerebalaneurysm or Swan Ganz catheter cannot have an MRI aneurysm or Swan Ganz catheter cannot have an MRI under any circumstances!

� Pregnancy is a contraindication and will require patient consent for an MRI.

� All other history of metal fragments in the eye require orbit screening x-rays prior to your MRI.

� All other history of implants or surgery must be indicated to the technologist. The make and model of implants may be necessary (i.e. ear implants, heart valve replacements).


Intravascular ultrasound (IVUS)


B-mode ultrasonography


Intravascular ultrasound (IVUS)

� Ultrasound -coronary artery;

� Endovascular ultrasound; ultrasound;

� Intravascular echocardiography


IVUS

� Alternative to injecting medium

� More reliable than angiography in indicating distribution and composition, arterial dissection, degree of stenosis of arterial dissection, degree of stenosis of the occluded artery


Intravascular ultrasound (IVUS)� A tiny ultrasound wand is attached to a

catheter. This ultrasound catheter is inserted into an artery in your groin area and moved up to the heart.and moved up to the heart.

� A computer measures how the sound waves reflect off blood vessels, and changes the sound waves into pictures.

� IVUS gives the health care provider a look at coronary arteries from the inside-out.


IVUS

� IVUS is almost always done at the end of angioplasty with stent placement, or coronary catheterization. Angioplasty gives a general look at the coronary arteries, but it cannot show the walls of the arteries. IVUS images show the artery walls and can reveal cholesterol and fat deposits (plaques). Buildup of these deposits can increase your risk of a heart attack.

� IVUS has provided a lot of insight into how stents become clogged (stent restenosis).


Let’s review


Diagnostic exams

� ECG

� Serum Markers of Myocardial Damage : Cardiac biomarkers

� Cardiac catheterization with coronary arteriographyarteriography

� Echocardiography

� Radionuclide imaging

� PET Scan

� CT scan

� Magnetic Resonance Imaging

� Intravascular ultrasound (IVUS)


Prognosis of CAD Prognosis of CAD


Prognosis of CAD Prognosis of CAD

�� >80 y/o = 60 %mortality>80 y/o = 60 %mortality

�� other diseases Dm, COPD= 30% other diseases Dm, COPD= 30% mortalitymortalitymortalitymortality

�� anterior wall MI= 30% mortalityanterior wall MI= 30% mortality


Health & Medicine

Nursing care of client with Coronary Artery Disease Part 1 of 2