CHAPTER 20
CARE OF PATIENTS WITH CORONARY ARTERY DISEASE AND
CARDIAC SURGERY
LESSON 20.1
CARE OF
PATIENTS WITH
CORONARY
ARTERY DISEASE
AND CARDIAC
SURGERY
THEORY
OBJECTIVES (1
OF 2)
Examine the risk factors of coronary
artery disease.
Illustrate the pathophysiology of
coronary artery disease.
Outline nursing interventions to care
for a patient experiencing angina,
including medication administration
and patient teaching.
THEORY OBJECTIVES (2
OF 2)
• EXPLAIN THE PATHOPHYSIOLOGY OF MYOCARDIAL
INFARCTION (MI).
• COMPARE AND CONTRAST THE SYMPTOMS OF AND
CARE FOR STABLE ANGINA WITH THOSE OF STEMI.
• DEVELOP A NURSING CARE PLAN FOR A PATIENT
EXPERIENCING AN MI.
• DEVELOP THE NURSING CARE OF A PATIENT
UNDERGOING CARDIAC SURGERY.
• DISCUSS FIVE COMPLICATIONS OF CARDIAC SURGERY.
CLINICAL PRACTICE
OBJECTIVES
• DEVELOP A TEACHING PLAN FOR A PATIENT
WITH CORONARY ARTERY DISEASE.
• IDENTIFY SIGNS AND SYMPTOMS THAT
INDICATE A PATIENT MAY BE EXPERIENCING A
MYOCARDIAL INFARCT.
• ADMINISTER MEDICATIONS TO PATIENTS
EXPERIENCING CARDIAC DISORDERS.
• COLLABORATE WITH OTHER HEALTH CARE
PROVIDERS TO CARE FOR PATIENTS AFTER
CARDIAC SURGERY
• CONTRIBUTE TO DISCHARGE PLANNING FOR
A PATIENT AFTER CARDIAC SURGERY.
About 630,000 people die of heart disease
in the United States every year–that's 1 in
every 4 deaths
Coronary heart disease (CHD) is the most
common type of heart disease, killing over
370,000 people annually
MI every 40 seconds
CARDIOVASCULAR
DISEASE
Costs about $200 billion each year - the cost
of health care services, medications, & lost
productivity
Risk factors – HTN, high LDL cholesterol, &
smoking – 49% have at least one risk factor
Other risk factors: Diabetes, overweight &
obesity, poor diet, physical inactivity,
excessive alcohol use
ARTERIOSCLEROSIS
• PATHOPHYSIOLOGY AND ETIOLOGY: LOSS
OF ELASTICITY OR HARDENING OF THE
ARTERIES THAT ACCOMPANIES THE AGING
PROCESS
• CAUSE
• CALCIUM IS DEPOSITED IN THE
CYTOPLASM CAUSING THE
ARTERIES TO LOSE ELASTICITY - LEFT
VENTRICLE CONTRACTS, RIGID
ARTERIAL VESSELS FAIL TO STRETCH
& THE RESULT IS A REDUCED
VOLUME OF OXYGENATED BLOOD
DELIVERED TO ORGANS SUCH AS
THE MYOCARDIUM, BRAIN,
KIDNEYS, & EXTREMITIES
ATHEROSCLEROSIS
• PATHOPHYSIOLOGY AND ETIOLOGY: A CONDITION
IN WHICH THE LUMEN OF THE ARTERIES FILL WITH
FATTY DEPOSITS (PLAQUE)
• PLAQUE IS CHIEFLY COMPOSED OF
CHOLESTEROL, WHICH IS A FATTY (LIPID)
SUBSTANCE
• ATHEROSCLEROSIS IS A MORE MODIFIABLE
CONTRIBUTOR THAN ARTERIOSCLEROSIS TO
VASCULAR DISEASE
• CONTRIBUTING RISK FACTORS THAT ARE
STUDIED
• MECHANISMS OF FAT FORMATION AND
METABOLISM
• OBESITY
• INFLAMMATORY RESPONSE
CAD
• CORONARY OCCLUSION: CLOSING OF A CORONARY ARTERY, WHICH
REDUCES OR TOTALLY INTERRUPTS BLOOD SUPPLY TO THE DISTAL
MUSCLE AREA
• CORONARY ARTERY DISEASE PRECEDES CORONARY OCCLUSION
• LEFT UNTREATED LEADS TO MYOCARDIAL INFARCTION (MI)
• SYMPTOMS USUALLY DO NOT OCCUR UNTIL AT LEAST 60% OF THE
ARTERIAL LUMEN IS OCCLUDED
Injury occurs to the endothelium over many yrs – may
be caused by tobacco use, hyperlipidemia, HTN,
obesity
Inflammation attracts macrophages which ingest lipids
and transport them into the arterial wall forming fatty
streaks
CORONARY
ARTERY
DISEASE
Macrophages release chemicals that damage lining
further and causes oxidation of low-density lipoprotein
(LDL) which is toxic to lining
Fibrous cap forms over deposits called an atheromas
or plaques
Plaques can become unstable, rupture, and attract
platelets causing thrombus formation – obstructing
blood flow leading to acute coronary syndrome (ACS)
May cause myocardial infarction (MI)
RISK FACTORS FOR CORONARY
ARTERY DISEASE (CAD)
Four modifiable risk factors cited as major (cholesterol abnormalities,
tobacco use, HTN, and diabetes)
Elevated LDL: primary target for cholesterol-lowering medication
Framingham risk calculator
Metabolic syndrome
hs-CRP (high-sensitivity C-reactive protein)
RISK
• OBESE AND APPLE-SHAPED BODY –
HIGHER RISK
• PULSE HIGH AT REST – IRREGULAR AT REST
• ARCUS SENILIS
• XANTHELASMA
• DIAGONAL CREASE IN THE EARLOBE AND
INCREASED RISK FOR CAD
ARCUS SENILIS
XANTHELASMA
BILATERAL
DIAGONAL
EARLOBE
CREASE
PREVENTION OF CAD
Control cholesterol
– LDL target >100
(>70 high risk)
Dietary measures –
Plant foods, less
red meat, fish
Physical activity –
Regular moderate
physical exercise –
stop if chest pain
Medications
Cessation of
tobacco use
Manage HTN
Control diabetes
SIGNS & SYMPTOMS OF
CAD
• SYMPTOMS ARE CAUSED BY MYOCARDIAL ISCHEMIA
& DEGREE OF SYMPTOMS & COMPLICATIONS ARE
RELATED TO THE LOCATION & DEGREE OF VESSEL
OBSTRUCTION
• CHEST DISCOMFORT, INCLUDING FEELING OF
TIGHTNESS, ACHING, & BURNING (ANGINA)
• CHEST PAIN RADIATING TO THE ARM, JAW, OR BACK
• DYSPNEA - PALPITATIONS OR TACHYCARDIA
• N/V - COLD, CLAMMY SKIN
• UNDUE FATIGUE (PARTICULARLY IN WOMEN)
• WEAKNESS & INABILITY TO COMPLETE USUAL
ACTIVITIES WITHOUT CHEST PAIN OR DYSPNEA
DIAGNOSIS
• ECG
• ECHOCARDIOGRAM
• CARDIAC STRESS TEST
• CARDIAC ANGIOGRAPHY
(CARDIAC
CATHETERIZATION),
• COMPUTED
TOMOGRAPHY (CT)
• ANGIOGRAM OR
MAGNETIC RESONANCE
ANGIOGRAM
LAB TESTS
• BLOOD GLUCOSE & HEMOGLOBIN A1C (HBA1C)
• LIPID PROFILE STUDIES
• LOW-DENSITY LIPOPROTEIN (LDL - “BAD CHOLESTEROL”)
HAS A LOWER RATIO OF PROTEIN TO CHOLESTEROL
• HIGH-DENSITY LIPOPROTEIN (HDL - “GOOD
CHOLESTEROL”) HAS A HIGHER RATIO OF PROTEIN TO
CHOLESTEROL
• TRIGLYCERIDES – CHAINS OF FATTY ACIDS
• ESTIMATED CARDIAC RISK - DIVIDE THE TOTAL SERUM
CHOLESTEROL LEVEL BY THE HDL LEVEL - A RESULT GREATER
THAN 5 SUGGESTS A POTENTIAL FOR CAD
STOP,
THINK,
AND
RESPOND
ALTHOUGH THE RECOMMENDED TOTAL
CHOLESTEROL LEVEL IS BELOW 200 MG/DL,
DETERMINE WHICH CLIENT HAS THE LOWEST
CARDIAC RISK BY DIVIDING TOTAL
CHOLESTEROL LEVEL BY HDL LEVEL AND
EXPLAIN YOUR ANSWER.
• CLIENT A: TOTAL CHOLESTEROL LEVEL IS
224 MG/DL; HDL LEVEL IS 38 MG/DL.
• CLIENT B: TOTAL CHOLESTEROL LEVEL IS 198
MG/DL; HDL LEVEL IS 35 MG/DL.
• CLIENT C: TOTAL CHOLESTEROL LEVEL IS 210
MG/DL; HDL LEVEL IS 55 MG/DL.
low-fat diet, weight
control, exercise - elevated
cholesterol & triglycerides
remain high
TREATMENT
lipid-lowering drugs
several herbs &
supplements Consult with
health care provider
before taking OTC
medications or herbs.
CHOLESTEROL
MEDICATIONS
• SIX TYPES OF LIPID-LOWERING AGENTS: AFFECT THE LIPID
COMPONENTS SOMEWHAT DIFFERENTLY (TABLE 23-1)
• HGMA-COA REDUCTASE INHIBITORS (STATINS)
ATORVASTATIN – LIPITOR, SIMVASTATIN – ZOCOR,
ROSUVASTATIN – CRESTOR
• NICOTINIC ACIDS - NIACIN
• FIBRIC ACIDS (OR FIBRATES) – FENOFIBRATE –
TRICOR, GEMFIBROZIL – LOPID
• BILE ACID SEQUESTRANTS (OR RESINS) –
CHOLESTYRAMINE - QUESTRAN
• CHOLESTEROL ABSORPTION INHIBITORS – EZETIMIBE
- EZETROL
• PCSK9 INHIBITORS: MONOCLONAL ANTIBODIES–
EVOLOCUMAB – REPATHA
CAD
• MEDICAL MANAGEMENT:
• WEIGHT LOSS, STRESS MANAGEMENT,
BLOOD GLUCOSE
• DRUG THERAPY: DRUG THERAPY TABLE PG.
420
• NITRATES – VASODILATION
• BETA-ADRENERGIC BLOCKERS &
CALCIUM CHANNEL BLOCKERS DECREASE HR
• ANGIOTENSIN-CONVERTING ENZYME
INHIBITORS & DIURETICS WITH
STRESS REDUCTION CONTROL HTN
Healthy lifestyle
Aspirin to prevent MI
NURSING
MANAGEMENT
Lower fat and cholesterol in the diet –
consult dietitian
Exercise
Weight control
Blood work to determine liver status if
on statins
A syndrome characterized by
episodes or paroxysmal pain or
pressure in the anterior chest caused
by insufficient coronary blood flow
Physical exertion or emotional stress
increases myocardial oxygen
demand, and the coronary vessels
are unable to supply sufficient blood
flow to meet the oxygen demand
ANGINA
PECTORIS
Types of angina
Stable or exertional: triggered by physical
activity or stress – relieved by rest and/or
nitroglycerine - goal is to reduce intensity &
frequency of attacks
TYPES OF
ANGINA
Variant: coronary artery spasms in normal
or diseased coronary arteries – chest pain
at rest – give nitrates or CCB - goal reduce
the number & severity of attacks
Unstable angina: usually caused by
occlusion of coronary arteries - pain occurs
even at rest - may not respond well to drug
therapy - may require immediate surgery
PAIN PATTERNS
• MAY BE DESCRIBED AS TIGHTNESS,
CHOKING, OR A HEAVY SENSATION
• FREQUENTLY RETROSTERNAL - MAY RADIATE
TO NECK, JAW, SHOULDERS, BACK OR ARMS
(USUALLY LEFT)
ASSESSMENT
AND
FINDINGS
FOR ANGINA
• ANXIETY FREQUENTLY ACCOMPANIES PAIN
• OTHER SYMPTOMS MAY OCCUR: DYSPNEA
OR SHORTNESS OF BREATH, DIZZINESS,
NAUSEA, VOMITING
• THE PAIN OF TYPICAL ANGINA SUBSIDES
WITH REST OR NTG
• UNSTABLE ANGINA IS CHARACTERIZED BY
INCREASED FREQUENCY & SEVERITY & NOT
RELIEVED BY REST NTG. REQUIRES MEDICAL
INTERVENTION!
PRECIPITATING FACTORS
• PHYSICAL EXERTION, WHICH PRECIPITATES AN
ATTACK BY INCREASING MYOCARDIAL
OXYGEN DEMAND
• EXPOSURE TO COLD, WHICH CAUSES
VASOCONSTRICTION AND ELEVATED BLOOD
PRESSURE, WITH INCREASED OXYGEN DEMAND
• EATING A HEAVY MEAL, WHICH INCREASES THE
BLOOD FLOW TO THE MESENTERIC AREA FOR
DIGESTION, THEREBY REDUCING THE BLOOD
SUPPLY AVAILABLE TO THE HEART MUSCLE; IN A
SEVERELY COMPROMISED HEART, SHUNTING
OF BLOOD FOR DIGESTION CAN BE
SUFFICIENT TO INDUCE ANGINAL PAIN
• STRESS OR ANY EMOTION-PROVOKING
SITUATION, CAUSING THE RELEASE OF
CATECHOLAMINES, WHICH INCREASES BLOOD
PRESSURE, HEART RATE, AND MYOCARDIAL
WORKLOAD
Diminished pain transition that occurs
with aging may affect presentation
of symptoms
OLDER
ADULT
CARE
POINTS
“Silent” CAD
Teach older adults to recognize their
“chest pain–like” symptoms (i.e.,
weakness)
Pharmacologic stress testing; cardiac
catheterization
Medications should be used
cautiously!
ECG changes indicative of
ischemia- T-wave inversion, STsegment elevation or development
of an abnormal Q wave
DIAGNOSIS
Stress testing, echocardiogram
TREATMENT
• DECREASE MYOCARDIAL OXYGEN DEMAND & INCREASE OXYGEN
• MEDICATIONS
• O2
• REDUCE & CONTROL RISK FACTORS
• REPERFUSION PROCEDURES
• PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY [PTCA]
• INTRACORONARY STENTS COATED WITH ANTI-INFLAMMATORY/ANTIBIOTIC
SUBSTANCE
• CABG
Nitroglycerin
Beta-adrenergic blocking agents
Calcium channel blocking agents
Antiplatelet and anticoagulant medications
Aspirin
Clopidogrel (Plavix)
MEDICATIONS
FOR ANGINA
Heparin
Ticlopidine (Ticlid)
OLDER ADULT CARE POINTS
Older adults are more sensitive to the
hypotensive effects of nitrates and
CCB’s - these drugs are used with
caution - assessing for orthostatic
blood pressure (BP) changes
following meals can help identify risk
for postprandial hypotension - during
digestion, blood flow diverts to the
GI tract
Peripheral vascular valve closure may
be sluggish in older adults, allowing
gravity to pull blood volume to the
lower extremities, resulting in
decreased cerebral blood flow and
increased potential for falls
PERCUTANEOUS TRANSLUMINAL
CORONARY ANGIOPLASTY (PTCA)
• AVOID LIFTING MORE THAN 10 LB FOR AT LEAST 3 DAYS IF
THE GROIN WAS USED FOR CATHETER INSERTION - AVOID
LIFTING MORE THAN 1 LB FOR AT LEAST 3 DAYS IF A SITE IN
THE UPPER EXTREMITY WAS USED
• REFRAIN FROM RIDING A BICYCLE, DRIVING A VEHICLE, OR
MOWING THE LAWN FOR AT LEAST 3 DAYS
• REFRAIN FROM SEXUAL ACTIVITY FOR 1 WEEK
• SHOWER RATHER THAN BATHE UNTIL THE SITE HEALS
CLINICAL
CLUES
PTCA
• CLEAN THE SITE WITH SOAP AND WATER, ELIMINATE ANY
DRESSING
• RELIEVE DISCOMFORT WITH A MILD ANALGESIC SUCH AS
ACETAMINOPHEN - NUMBNESS AT THE SITE IS TEMPORARY
AND NOT UNUSUAL
• EXPECT TO SEE A BRUISE, WHICH MAY LAST 1–3 WEEKS, AT
THE CATHETER INSERTION SITE.
• REPORT ANY SIGNS OF BLEEDING, INFECTION, OR IMPAIRED
CIRCULATION
• NOTIFY THE CARDIOLOGIST IMMEDIATELY IF THERE IS PAIN
OR TIGHTNESS IN THE CHEST, WHICH COULD INDICATE
OBSTRUCTED BLOOD FLOW THROUGH THE CORONARY
ARTERY.
NURSING INTERVENTIONS
FOR THE PATIENT WITH
ANGINA PECTORIS
• TREAT ANGINA
• REDUCE ANXIETY
• PREVENT PAIN
• EDUCATE PATIENTS ABOUT SELF-CARE
• CONTINUING CARE
NURSING
INTERVENTION:
TREAT ANGINA
• PRIORITY
• PATIENT IS TO STOP ALL ACTIVITIES AND SIT OR REST
IN BED (SEMI-FOWLER POSITIONING)
• ASSESS THE PATIENT WHILE PERFORMING OTHER
NECESSARY INTERVENTIONS. ASSESSMENT INCLUDES
VS, OBSERVATION FOR RESPIRATORY DISTRESS, AND
ASSESSMENT OF PAIN. IN THE HOSPITAL SETTING, THE
ECG IS ASSESSED OR OBTAINED
• ADMINISTER MEDICATIONS AS ORDERED OR BY
PROTOCOL, USUALLY NTG. REASSESS PAIN AND
ADMINISTER NTG UP TO THREE DOSES
• ADMINISTER OXYGEN 2 L/MIN BY NASAL CANNULA
Use a calm manner
Stress-reduction techniques
NURSING
INTERVENTION:
REDUCE
ANXIETY
Patient teaching
Addressing patient’s spiritual needs may
assist in allaying anxieties
Address both patient and family needs
NURSING INTERVENTION:
PREVENTING PAIN
• IDENTIFY LEVEL OF ACTIVITY THAT CAUSES
PATIENT’S PRODROMAL S&S
• PLAN ACTIVITIES ACCORDINGLY
• ALTERNATE ACTIVITIES WITH REST PERIODS
• EDUCATE PATIENT AND FAMILY
NURSING
INTERVENTION:
PATIENT
TEACHING #1
Balance
Balance activity with rest
Follow
Follow prescribed exercise regimen
Avoid
Avoid exercising in extreme temperatures
Use
Use resources for emotional support (counselor)
Avoid
over
Avoid over-the-counter medications that may increase
HR or BP before consulting with health care provider
Stop
Stop using tobacco products (nicotine increases HR
and BP)
Diet
Diet low in fat and high in fiber
Medication teaching (carry
NTG at all times!)
NURSING
INTERVENTION:
PATIENT
TEACHING #2
Follow up with health care
provider
Report increase in S&S to
provider
Maintain normal BP and blood
glucose levels
PLANNING AND
GOALS FOR THE
PATIENT WITH
ANGINA PECTORIS
GOALS
• IMMEDIATE AND APPROPRIATE
TREATMENT OF ANGINA
• PREVENTION OF ANGINA
• REDUCTION OF ANXIETY
• AWARENESS OF THE DISEASE
PROCESS
• UNDERSTANDING OF
PRESCRIBED CARE AND
ADHERENCE TO THE SELFCARE PROGRAM
• ABSENCE OF
COMPLICATIONS
• FOR SUBLINGUAL NITROGLYCERIN:
• SIT DOWN AND REST BEFORE SELF-ADMINISTERING
NITROGLYCERIN. DECREASED ACTIVITY MAY RELIEVE CHEST
PAIN; SITTING WILL PREVENT INJURY SHOULD THE
NITROGLYCERIN LOWER BP AND CAUSE FAINTING
• PLACE ONE NITROGLYCERIN TABLET UNDER THE TONGUE IF
2–3 MINUTES OF REST FAILS TO RELIEVE PAIN
• EXPECT TO FEEL DIZZY, FLUSHED OR TO DEVELOP AN H/A
CLINICAL
CLUES
• LET THE TABLET DISSOLVE SLOWLY - THERE SHOULD BE
SLIGHT TINGLING OR BURNING UNDER THE TONGUE.
• TAKE A SECOND IN 5 MINUTES IF CHEST PAIN STILL THERE TAKE A THIRD IN 5 MORE MINUTES IF CHEST PAIN STILL
THERE
• CALL 911 IF CHEST PAIN CONTINUES; DO NOT DRIVE TO AN
ED • KEEP A FEW NITROGLYCERIN TABLETS IN A DARK, DRY
CONTAINER WITH YOU AT ALL TIMES; CONSULT WITH THE
PHARMACIST ABOUT A SEALED METAL CONTAINER THAT
YOU CAN WEAR AROUND THE NECK.
• DO NOT PLACE OTHER MEDICATIONS IN THE CONTAINER
• REPLACE NITROGLYCERIN TABLETS EVERY 6 MONTHS OR
AFTER ANY CONTAINER HAS BEEN OPENED SIX TIMES
• NITROGLYCERIN SPRAY:
• ASSUME A SITTING POSITION AND HOLD THE
CANISTER UPRIGHT
• SPRAY THE NITROGLYCERIN ONTO THE TONGUE
WITHOUT INHALING.
• CLOSE THE MOUTH IMMEDIATELY AFTERWARD
CLINICAL
CLUES
• EXPECT TO FEEL DIZZY OR FLUSHED OR TO DEVELOP
A HEADACHE
• REPEAT SPRAY EVERY 5 MINUTES FOR A SECOND
AND THIRD TIME IF CHEST PAIN IS UNRELIEVED.
• CALL 911 IF CHEST PAIN CONTINUES.
• EXPECT A NEW CANISTER OF NITROGLYCERIN TO
DELIVER APPROXIMATELY 200 DOSES.
• CHECK THE AMOUNT OF NITROGLYCERIN IN THE
CANISTER BY FLOATING IT IN A BOWL OF WATER;
THE HIGHER THE CANISTER FLOATS, THE LESS
MEDICATION IT CONTAINS
AUDIENCE RESPONSE
QUESTION
THE NURSE IS CARING FOR A PATIENT WHO HAS
SEVERE CHEST PAIN AFTER WORKING OUTSIDE ON A
HOT DAY AND IS BROUGHT TO THE EMERGENCY
CENTER. THE NURSE ADMINISTERS NITROGLYCERIN TO
HELP ALLEVIATE CHEST PAIN. WHICH SIDE EFFECT
SHOULD CONCERN THE NURSE THE MOST?
A.
DRY MUCOUS MEMBRANES
B.
HEART RATE OF 88 BPM
C.
BLOOD PRESSURE OF 86/58 MM HG
D.
COMPLAINTS OF HEADACHE
ANSWER
C. BLOOD PRESSURE OF 86/58 MM HG
RATIONALE: NITROGLYCERIN DILATES VESSELS IN THE
BODY. DILATION OF THE VEINS CAUSES VENOUS
POOLING OF BLOOD THROUGHOUT THE BODY. AS
A RESULT, LESS BLOOD RETURNS TO THE HEART, AND
FILLING PRESSURE (PRELOAD) IS REDUCED. IF THE
PATIENT IS HYPOVOLEMIC, THE DECREASE IN FILLING
PRESSURE CAN CAUSE A SIGNIFICANT DECREASE IN
CARDIAC OUTPUT AND BLOOD PRESSURE. THIS
PATIENT WAS WORKING OUTSIDE ON A HOT DAY,
AND THE POSSIBILITY OF DEHYDRATION AND
HYPOVOLEMIA SHOULD BE CONSIDERED. DRY
MUCOUS MEMBRANES CAN CAUSE POOR
ABSORPTION OF SUBLINGUAL NITROGLYCERIN BUT
IS NOT THE MOST CONCERNING. B AND D ARE
INSIGNIFICANT FINDINGS.
ACS/MI FACTS
About 805,000 Americans experience an MI annually
366,000 die from MI (AHA, 2020c)
heart disease rising in all populations - Women more
likely to experience heart attacks after menopause poor diet, sedentary lifestyle, increased levels of
stress contribute to development of cvd earlier in life
for an increasing number of women
ACUTE CORONARY SYNDROME
(ACS) AND MYOCARDIAL
INFARCTION (MI)
• EMERGENT SITUATION
• CHARACTERIZED BY AN ACUTE ONSET OF
MYOCARDIAL ISCHEMIA THAT RESULTS IN
MYOCARDIAL DEATH (I.E., MI) IF DEFINITIVE
INTERVENTIONS DO NOT OCCUR PROMPTLY
• ALTHOUGH THE TERMS CORONARY
OCCLUSION, HEART ATTACK, AND MI ARE
USED SYNONYMOUSLY, THE PREFERRED TERM
IS MI
PATHOPHYSIOLOGY
• PLAQUE RUPTURE - THROMBUS FORMATION - COMPLETE OCCLUSION
OF THE ARTERY - ISCHEMIA & NECROSIS OF THE MYOCARDIUM
SUPPLIED BY THAT ARTERY
• OTHER CAUSES OF MI - VASOSPASM OF CORONARY ARTERY,
DECREASED OXYGEN SUPPLY, OR INCREASED DEMAND FOR OXYGEN
• PROFOUND IMBALANCE BETWEEN MYOCARDIAL O2 SUPPLY AND
DEMAND
• AREA OF INFARCTION - CELLS DEPRIVED OF O2, ISCHEMIA DEVELOPS,
CELLULAR INJURY OCCURS, LACK OF O2 RESULTS IN INFARCTION
• “TIME IS MUSCLE” REFLECTS URGENCY OF APPROPRIATE TREATMENT TO
IMPROVE OUTCOMES
• APPROXIMATELY EVERY 40 SECONDS, SOMEONE WILL HAVE AN
MI - MANY WILL DIE - EARLY RECOGNITION & TREATMENT
IMPROVE SURVIVAL
• MYOCARDIAL DAMAGE CAUSES CELL TO LOSE AUTOMATICITY,
EXCITABILITY, CONDUCTIVITY, CONTRACTILITY, AND RHYTHMICITY
Identify an MI
PATHOPHYSIOLOGY
• Type: NSTEMI or STEMI - determined by
diagnostic tests
• Location of injury to the ventricular wall: anterior,
inferior, posterior, or lateral wall
• Point in time within the process of infarction:
acute, evolving, or old
12-lead ECG identifies type & location
of the MI - Q wave & patient history
identify the timing
Goals of medical therapy - relieve
symptoms, prevent or minimize
myocardial tissue death, prevent
complications
CLINICAL MANIFESTATIONS
Sudden chest pain – continues despite rest & meds
Some have prodromal symptoms or previous dx of CAD others no previous symptoms
Symptoms: chest pain, shortness of breath, indigestion,
nausea, anxiety
Sympathetic NS - cool, pale, & moist skin, HR & R may be
elevated – may be short lived or remain
Sometimes S/S may not be distinguished from unstable
angina - the evolution of the term acute coronary syndrome
MI
• MYOCARDIUM INJURY
• INFLAMMATORY RESPONSE
• DAMAGED CELLS RELEASE SERUM
CARDIAC MARKERS & ELECTROLYTES
• LOSS OF INTRACELLULAR POTASSIUM
& LACTIC ACID FROM ANAEROBIC
METABOLISM AFFECT
DEPOLARIZATION AND
REPOLARIZATION CAUSING
DANGEROUS ARRHYTHMIAS
• MYOCARDIUM INJURY
• INFLAMMATORY RESPONSE
• DAMAGED CELLS RELEASE SERUM
CARDIAC MARKERS & ELECTROLYTES
• LOSS OF INTRACELLULAR POTASSIUM
& LACTIC ACID FROM ANAEROBIC
METABOLISM AFFECT
DEPOLARIZATION AND
REPOLARIZATION CAUSING
DANGEROUS ARRHYTHMIAS
MI
EFFECTS OF ISCHEMIA, INJURY,
AND INFARCTION ON ECG
ZONES OF MYOCARDIAL
INFARCTION
Symptoms and activities, especially
those that precede and precipitate
attack
ASSESSMENT
Health Hx - description of the
presenting symptom, hx previous
cardiac and other illnesses, family
hx heart disease, risk factors
Symptoms and activities, especially those
that precede and precipitate attack
ASSESSMENT
Health Hx - description of the presenting
symptom, hx previous cardiac and other
illnesses, family hx heart disease, risk factors
Time to prevent significant myocardial
damage narrow
Sooner medical treatment started - greater
chance of saving myocardium & preserving
life
ASSESSMENT
Cardiovascular
Chest pain not relieved by rest or NTG, palpitations, S3, S4, & new onset of murmur
Increased JVD if the myocardial infarction (MI) has caused heart failure
BP may be elevated because of sympathetic stimulation or decreased because of decreased contractility
impending cardiogenic shock, or medications
Irregular pulse may indicate atrial fibrillation
May have ST-segment & T-wave changes- the ECG may show tachycardia, bradycardia, or other arrhythmia
Respiratory
Shortness of breath, dyspnea, tachypnea, and crackles if MI has caused pulmonary congestion - Pulmonary
edema may be present
Gastrointestinal
Nausea, indigestion, and vomiting
ASSESSMENT
• GENITOURINARY
• DECREASED URINARY OUTPUT MAY INDICATE CARDIOGENIC SHOCK
• SKIN
• COOL, CLAMMY, DIAPHORETIC, PALE APPEARANCE DUE TO SYMPATHETIC
STIMULATION MAY INDICATE CARDIOGENIC SHOCK.
• NEUROLOGIC
• ANXIETY, RESTLESSNESS, AND LIGHTHEADEDNESS MAY INDICATE INCREASED
SYMPATHETIC STIMULATION OR A DECREASE IN CONTRACTILITY AND
CEREBRAL OXYGENATION - MAY ALSO INDICATE CARDIOGENIC SHOCK.
• PSYCHOLOGICAL
• FEAR WITH FEELING OF IMPENDING DOOM, OR DENIAL THAT ANYTHING IS
WRONG.
WOMEN
May complain of recent
episodes of extreme fatigue,
with inability to complete daily
activities without prolonged
rest periods - may have chest
pressure, followed by eventual
return to a full energy state
Feelings of indigestion are
common
Atypical symptoms - sharp
pain, fatigue, weakness
Denial is a significant factor in
not seeking quick treatment
Ccan lead to increased heart
damage
OLDER ADULTS
FATIGUE
SYNCOPE
(TEMPORARY LOSS OF
CONSCIOUSNESS)
WEAKNESS
DIAGNOSTICS
• 12-LEAD ECG – R/O OR DIAGNOSE AN ACUTE MI OBTAINED WITHIN 10 MINUTES FROM TIME
PATIENT REPORTS PAIN OR ARRIVES IN THE ED – BY
MONITORING SERIAL ECG CHANGES OVER TIME,
THE LOCATION, EVOLUTION, AND RESOLUTION OF
AN MI CAN BE IDENTIFIED AND MONITORED
• ECHOCARDIOGRAM EVALUATES VENTRICULAR
FUNCTION - USED TO ASSIST IN DIAGNOSING AN
MI WHEN THE ECG IS NONDIAGNOSTIC - DETECTS
HYPOKINETIC AND AKINETIC WALL MOTION AND
CAN DETERMINE THE EJECTION FRACTION
• CHEST X-RAY WILL RULE OUT OTHER POSSIBLE
CAUSES
LABORATORY TESTS
• TROPONIN - TROPONINS I AND T SPECIFIC FOR CARDIAC MUSCLE – RELIABLE
& CRITICAL MARKERS OF MYOCARDIAL INJURY - CAN BE DETECTED WITHIN A
FEW HOURS & REMAINS ELEVATED FOR AS LONG AS 2 WEEKS - DETECTS
INFLAMMATION & OTHER FORMS OF MECHANICAL STRESS ON MYOCARDIUM
SUCH AS SEPSIS, HEART FAILURE, & RESPIRATORY FAILURE
• CREATINE KINASE AND ITS ISOENZYMES - CK-MM (SKELETAL MUSCLE), CK-MB
(HEART MUSCLE), CK-BB (BRAIN TISSUE) - CK-MB CARDIAC-SPECIFIC
ISOENZYME - FOUND MAINLY IN CARDIAC CELLS & INCREASES WITH
DAMAGE TO THESE CELLS - ELEVATED CK-MB IS AN INDICATOR OF ACUTE MI LEVEL BEGINS TO RISE WITHIN A FEW HOURS & PEAKS WITHIN 24 HOURS OF
AN INFARCT
• MYOGLOBIN - HEME PROTEIN THAT HELPS TRANSPORT O2 - FOUND IN
CARDIAC & SKELETAL MUSCLE - START TO RISE WITHIN 1 TO 3 HOURS AND
PEAKS WITHIN 12 HOURS AFTER ONSET OF SYMPTOMS BUT NOT VERY
SPECIFIC IN INDICATING AN ACUTE CARDIAC EVENT BUT NEGATIVE RESULTS
CAN R/O AN ACUTE MI
INITIAL MANAGEMENT
• SUSPECTED MI SHOULD IMMEDIATELY RECEIVE
• MONA – MORPHINE, OXYGEN, NTG, ASPIRIN
• MORPHINE IS DRUG OF CHOICE - REDUCE PAIN,
ANXIETY - REDUCES PRELOAD & AFTERLOAD - MONITOR
CAREFULLY FOR HYPOTENSION OR DECREASED
RESPIRATORY RATE (POTENTIAL ADVERSE OUTCOMES INCLUDING LARGER INFARCT SIZE, INCREASED LENGTH
OF HOSPITAL STAY & MORTALITY
• BETA-BLOCKER IF ARRHYTHMIAS OCCUR - IF NOT NEEDED
IN INITIAL MANAGEMENT - SHOULD BE GIVEN WITHIN 24
HRS IF NO CONTRAINDICATIONS
• UNFRACTIONATED HEPARIN OR LMWH MAY BE
PRESCRIBED ALONG WITH PLATELET-INHIBITING AGENTS
TO PREVENT FURTHER CLOT FORMATION
MEDICAL MANAGEMENT
• GOALS: MINIMIZE MYOCARDIAL DAMAGE,
PRESERVE MYOCARDIAL FUNCTION,
PREVENT COMPLICATIONS
• MINIMIZE MYOCARDIAL DAMAGE – REDUCE
MYOCARDIAL O2 DEMAND & INCREASE O2
SUPPLY WITH MEDICATIONS, O2, BED REST
• RESOLUTION OF PAIN & ECG
CHANGES INDICATE DEMAND &
SUPPLY ARE IN EQUILIBRIUM - INDICATE
REPERFUSION
• VISUALIZATION OF BLOOD FLOW
DURING CATHETERIZATION IN CATH
LAB IS EVIDENCE OF REPERFUSION
EMERGENT
PERCUTANEOUS
CORONARY
INTERVENTION
• PATIENT WITH STEMI TAKEN DIRECTLY TO THE
CARDIAC CATH LAB FOR AN IMMEDIATE PCI IF
POSSIBLE - USED TO OPEN OCCLUDED
CORONARY ARTERY & PROMOTE REPERFUSION PCI PREFERRED INITIAL TREATMENT FOR ACUTE MI
IN ALL AGE GROUPS
• TREATS UNDERLYING ATHEROSCLEROTIC LESION
• DURATION OF O2 DEPRIVATION DETERMINES
NUMBER OF MYOCARDIAL CELLS THAT DIE - TIME
FROM THE PATIENT’S ARRIVAL IN THE ED TO THE
TIME PCI IS PERFORMED SHOULD BE LESS THAN
60 MINUTES – “DOOR-TO-BALLOON TIME”
THROMBOLYTICS
Thrombolytic therapy initiated when primary PCI not
available or transport time to a PCI-capable hospital is
too long
Administered IV - used most often are alteplase, reteplase,
Tenecteplase
Purpose - dissolve the thrombus (thrombolysis)- allowing
reperfusion - minimizing size of infarction & preserving
ventricular function
Do not affect underlying atherosclerotic lesion - may be
referred for a cardiac catheterization and other invasive
procedures following the use of thrombolytic therapy
Should not be used if patient is bleeding or has a
bleeding disorder
Should be given within 30 minutes of symptom onset for
best results – “door-to-needle time”
INDICATIONS FOR THROMBOLYTIC
THERAPY
Chest pain lasting more than 20 minutes,
unrelieved by nitroglycerin
ST-segment elevation in at least two leads
that face the same area of the heart
Less than 12 hours from onset of pain
ABSOLUTE CONTRAINDICATIONS FOR
THROMBOLYTIC THERAPY
Active bleeding
Known bleeding disorder
History of hemorrhagic stroke
History of intracranial vessel malformation
Recent major surgery or trauma
Uncontrolled hypertension
Pregnancy
NURSING CONSIDERATIONS
• MINIMIZE NUMBER OF TIMES THE PATIENT’S SKIN IS PUNCTURED
• AVOID INTRAMUSCULAR INJECTIONS
• DRAW BLOOD FOR LABORATORY TESTS WHEN STARTING THE IV LINE
• START IV LINES BEFORE THROMBOLYTIC THERAPY; DESIGNATE ONE LINE TO USE FOR BLOOD
DRAWS
• AVOID CONTINUAL USE OF NONINVASIVE BLOOD PRESSURE CUFF
• MONITOR FOR ACUTE ARRHYTHMIAS & HYPOTENSION
• MONITOR FOR REPERFUSION: RESOLUTION OF ANGINA OR ACUTE ST-SEGMENT CHANGES
• CHECK S/S OF BLEEDING: DECREASE IN H&H & BP, INCREASE HR, OOZING OR BULGING AT
INVASIVE PROCEDURE SITES, BACK PAIN, MUSCLE WEAKNESS, CHANGES IN LOC, C/O H/A
• TREAT MAJOR BLEEDING BY DISCONTINUING THROMBOLYTIC THERAPY & ANY
ANTICOAGULANTS - APPLY DIRECT PRESSURE & NOTIFY THE PRIMARY PROVIDER IMMEDIATELY TREAT MINOR BLEEDING BY APPLYING DIRECT PRESSURE IF ACCESSIBLE & APPROPRIATE CONTINUE TO MONITOR
INPATIENT MANAGEMENT
• CONTINUOUS CARDIAC MONITORING
• PHARMACOLOGIC MANAGEMENT – ASA, BETABLOCKER, ACE INHIBITOR - DECREASES BP & DIURESIS
OCCURS DECREASING O2 DEMAND OF THE HEART DECREASES MORTALITY RATES - PREVENTS
REMODELING OF MYOCARDIAL CELLS ASSOCIATED
WITH ONSET OF HEART FAILURE
• MONITOR BP, URINE OUTPUT, SERUM SODIUM,
POTASSIUM, AND CREATININE LEVELS
• NICOTINE REPLACEMENT THERAPY & TOBACCO
CESSATION COUNSELING SHOULD INITIATED FOR ALL
TOBACCO USERS
• ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITOR
OR ANGIOTENSIN RECEPTOR BLOCKER (ARB) THERAPY
AT DISCHARGE FOR LEFT VENTRICULAR EJECTION
FRACTION LESS THAN 40%
CARDIAC REHABILITATION
The goals of rehabilitation - extend
& improve quality of life - limit the
effects & progression of
atherosclerosis, return the patient to
work & pre-illness lifestyle, enhance
patient’s psychosocial & vocational
status, prevent another cardiac
event3 phases
Phase 1 – begins in the hospital
with education
Phase 3 – long-term outpatient –
focuses on maintaining CV stability
& long-term conditioning – usually
self-directed
Phase 2 – 3x/wk for 4-6 wks or up
to 6 months – supervised exercise,
education
Denial
EMOTIONAL
AND
BEHAVIORAL
RESPONSES
TO ACUTE
MYOCARDIAL
INFARCTION
Anger
Anxiety and fear
Dependency
Depression
Realistic acceptance
• AREA OF MAJOR CONCERN - MAY BE FEARFUL OF
RESUMING SEXUAL ACTIVITY
• MAY CAUSE ANOTHER MI – PARTNER MAY ALSO FEAR
• NEEDS REASSURANCE THAT RESUMPTION OF NORMAL
SEXUAL ACTIVITIES WILL BE POSSIBLE
SEXUALITY
• MAY NEED EDUCATION REGARDING TIMING –. CAN CLIMB A
FLIGHT OF STAIRS WITHOUT MUCH CHANGE IN HR, R, BP
SHOULD NOT BE ANY SIGNIFICANT STRESS ON THE HEART
HEALTH CARE PROVIDER SHOULD DISCUSS WITH PATIENT &
PARTNER, IF PROVIDER DOES NOT, ENSURE THAT THE PROPER
INFORMATION IS GIVEN
• SEXUAL DYSFUNCTION MAY BE A SIDE EFFECT OF SOME
MEDICATIONS
• PLAN FOR TIMES WHEN WELL RESTED & AVOID AN
ENVIRONMENT THAT IS TOO HOT OR TOO COLD - AT LEAST
2 HOURS AFTER EATING OR DRINKING ALCOHOL
• NTG SHOULD BE USED PROPHYLACTICALLY IF SEXUAL
ACTIVITY CAUSES ANGINA – IF SYMPTOMS. OCCUR, CEASE
ACTIVITY, PLACE A NITROGLYCERIN TABLET UNDER THEIR
TONGUE, LIE DOWN, & REST.
PLANNING AND GOALS
FOR THE PATIENT WITH
ACS
• GOALS:
• RELIEF OF PAIN OR ISCHEMIC SIGNS (E.G.,
ST-SEGMENT CHANGES) AND SYMPTOMS
• PREVENTION OF MYOCARDIAL DAMAGE
• MAINTENANCE OF EFFECTIVE RESPIRATORY
FUNCTION, ADEQUATE TISSUE PERFUSION
• REDUCTION OF ANXIETY
• ADHERENCE TO THE SELF-CARE PROGRAM
• EARLY RECOGNITION OF COMPLICATIONS
NURSING
INTERVENTIONS
FOR THE PATIENT
WITH ACS
Relieve
Relieve pain and S&S of ischemia
Improve
Improve respiratory function
Promote
Promote adequate tissue perfusion
Reduce
Reduce anxiety
Monitor and
manage
Monitor and manage potential
complications
Educate
Educate patient and family
Provide
Provide continuing care
NURSING MANAGEMENT
OF THE PATIENT WITH
ACS
• OXYGEN AND MEDICATION THERAPY
• FREQUENT VS ASSESSMENT
• PHYSICAL REST IN BED WITH HEAD OF BED ELEVATED
• RELIEF OF PAIN HELPS DECREASE WORKLOAD OF
HEART
• MONITOR I&O AND TISSUE PERFUSION
• FREQUENT POSITION CHANGES TO PREVENT
RESPIRATORY COMPLICATIONS
• REPORT CHANGES IN PATIENT’S CONDITION
• EVALUATE INTERVENTIONS!
Dysrhythmia
Heart failure
SIGNS AND
SYMPTOMS OF
COMPLICATIONS
AFTER
MYOCARDIAL
INFARCTION
Cardiogenic shock
Papillary muscle dysfunction
Ventricular aneurysm
Pericarditis
Dressler syndrome
AUDIENCE
RESPONSE
QUESTION
The nurse is caring for a patient
after cardiac surgery. Which
nursing intervention is
appropriate to help prevent
complications arising from
venous stasis?
• Encourage crossing of legs
• Use pillows in the popliteal space to
elevate the knees in the bed
• Discourage exercising
• Apply sequential pneumatic
compression devices as prescribed
D. Apply sequential pneumatic compression devices as
prescribed
ANSWER
Rationale: Sequential pneumatic compression devices
should be used when prescribed to help prevent
venous stasis and clotting complications such as deep
vein thrombosis and pulmonary embolism. Patients
should be discouraged to cross their legs. Pillows
should not be used in the popliteal space to elevate
the knees; rather, this should be avoided. Exercises,
passive and active, should be encouraged.
PCI
• ATHERECTOMY
• PERCUTANEOUS TRANSLUMINAL
CORONARY ANGIOPLASTY (PTCA)
• CORONARY ARTERY STENT
• CORONARY ARTERY BYPASS GRAFT (CABG)
• CARDIAC SURGERY
ARTHERECTOMY
Balloon-tipped catheter is used
to open blocked coronary
vessels and resolve ischemia
Used to tx patients with angina
and as an intervention for ACS
or to open blocked CABGs
PERCUTANEOUS
CORONARY
INTERVENTION
Purpose is to improve blood
flow within a coronary artery
by compressing the atheroma
PERCUTANEOUS CORONARY
INTERVENTION
CABG
• CORONARY ARTERY BYPASS
GRAFT SURGERY (CABG)
• LEG VEIN OR CHEST ARTERY
HARVESTED – MID-STERNAL
INCISION CLOSED WITH
WIRE – HEART IS STOPPED
AND CLIENT PLACED ON
BYPASS – MAY HAVE MORE
THAN 1 GRAFT – HEART
RESTARTED
CARDIOPULMONARY
BYPASS
• CPB - EXTRACORPOREAL CIRCULATION - MECHANICALLY
CIRCULATES & OXYGENATES BLOOD WHILE BYPASSING THE
HEART & LUNGS – PROVIDES A MOTIONLESS, BLOODLESS
SURGICAL FIELD
• A CANNULA IS PLACED IN THE RIGHT ATRIUM, VENA CAVA,
OR FEMORAL VEIN TO WITHDRAW BLOOD - CANNULA IS
CONNECTED TO TUBING FILLED WITH AN ISOTONIC
CRYSTALLOID SOLUTION - THE VENOUS BLOOD IS FILTERED,
OXYGENATED, COOLED OR WARMED BY THE MACHINE, AND
THEN RETURNED TO THE BODY - THE CANNULA USED TO
RETURN THE OXYGENATED BLOOD IS USUALLY INSERTED IN
THE ASCENDING AORTA OR FEMORAL ARTERY - HEART IS
STOPPED BY THE INJECTION OF A POTASSIUM-RICH
CARDIOPLEGIA SOLUTION INTO THE CORONARY ARTERIES HEPARIN IS GIVEN TO PREVENT CLOTTING AND THROMBUS
FORMATION IN THE BYPASS CIRCUIT - AT THE END OF THE
PROCEDURE WHEN THE PATIENT IS DISCONNECTED FROM
THE BYPASS MACHINE, PROTAMINE SULFATE IS GIVEN TO
REVERSE THE EFFECTS OF HEPARIN
Hypothermia is maintained at about
82.4°F
Blood is cooled & returned to the
body which slows BMR decreasing O2
demand
CARDIOPULMONARY
BYPASS
At surgical completion blood is
rewarmed as it passes through the
CPB circuit
Urine output, arterial blood gases,
electrolytes, coagulation studies
monitored to assess status during CPB
CORONARY ARTERY BYPASS
GRAFTS
VEINS COMMONLY USED FOR
BYPASS GRAFT PROCEDURES
CARDIOPULMONARY BYPASS
SYSTEM
OFF-PUMP CORONARY ARTERY
BYPASS (OPCAB)
Beta-adrenergic blocker
used to slow HR
Myocardial stabilization
device to hold the site still
for the anastomosis of the
bypass graft into the
coronary artery while the
heart continues to beat
STABILIZER DEVICE
POST-OP PATIENT
CARDIOGENIC SHOCK
• LEFT VENTRICLE IS BADLY DAMAGED, CARDIOGENIC SHOCK
MAY OCCUR
• SIGNS AND SYMPTOMS ARE THOSE THAT ACCOMPANY
DECREASED CARDIAC OUTPUT
• SIGNS AND SYMPTOMS
• CONFUSION; RESTLESSNESS; DIAPHORESIS; RAPID, THREADY
PULSE; INCREASED RESPIRATORY RATE; COLD, CLAMMY SKIN;
DIMINISHING URINARY OUTPUT TO LESS THAN 20 ML/H
IMMEDIATE CARE
INTRA-AORTIC BALLOON PUMP (IABP)
• USES A BALLOON CATHETER POSITIONED IN THE AORTA THAT INFLATES
DURING DIASTOLE AND DEFLATES DURING SYSTOLE, EFFECTIVELY
DECREASING THE WORKLOAD OF THE HEART AND INCREASING BLOOD
FLOW THROUGH THE CORONARY ARTERIES (DISCUSSED IN CHAPTER 19)
HEART TRANSPLANTATION
Causes: cardiomyopathy, endstage coronary artery disease,
end-stage heart failure, in
neonates and infants severe
congenital cardiac defects
National Organ Transplant Act
(1984) outlawed the sale of
human organs
More than 2300 transplants
and almost double the need
United Network for Organ
Sharing – Box 29-2, pg. 493
HEART TRANSPLANTATION
Transplant must be transplanted
within 6 hours of removal
Two methods:
Orthotopic – leaves back half of both atria
Heterotropic – rare – original heart left in
place, allows for heart function with lifethreatening rejection
HEART TRANSPLANTATION
• SCARCITY: ORGANS—20% OF 3,000 PEOPLE AWAITING HEART TRANSPLANT DIE
BEFORE DONOR BECOMES AVAILABLE – ONLY 1 IN 3 DONOR HEARTS ARE
ACCEPTED
• THE IDEAL DONOR IS YOUNG, FIT, HEALTHY, AND DIES SUDDENLY
• FEW POSSESS DOCUMENTED CONSENT FOR ORGAN DONATION - NEXT
OF KIN ARE RELUCTANT TO DONATE WHEN CLIENT APPEARS TO BE ALIVE
WITH MACHINES
• NO FINANCIAL INCENTIVES TO DONATE HEART OR OTHER ORGAN
• PHYSICIANS DELAY DISCUSSING ORGAN DONATION WITH THE FAMILY OF
POTENTIAL DONORS WHILE THEY ATTEMPT MORE AND MORE
SOPHISTICATED MEASURES TO KEEP DYING CLIENTS ALIVE WHILE THE
QUALITY OF ORGANS DECLINE
HEART TRANSPLANTATION
• STRINGENT CRITERIA FOR DONATED ORGANS RESULTS IN THE REJECTION OF
MARGINAL HEARTS FROM OLDER DONORS WITH VARIOUS COMORBIDITIES THAT
COULD LOWER THE RISK OF DEATH AMONG POTENTIAL RECIPIENTS AS
COMPARED TO PROLONGING THE WAIT FOR A HIGHER QUALITY HEART
• A FALSE BELIEF THAT ORGAN DONATION WILL INTERFERE WITH A TRADITIONAL
OPEN CASKET FUNERAL
• SOME CULTURAL GROUPS, SUCH AS AFRICAN AMERICANS AND HISPANICS, ARE
LESS LIKELY TO DONATE ORGANS WHICH REDUCES THE POTENTIAL FOR
MATCHING HUMAN LEUKOCYTE ANTIGEN (HLA) TYPES WITH SOMEONE FROM
THE SAME ETHNIC BACKGROUND
• SOME CULTURES AND RELIGIONS ADVANCE A BELIEF THAT A PERSON SHOULD DIE
WITH ALL ORGANS INTACT (SIE, 2015).
• TRANSPLANT PROBLEMS:
• REJECTION—HYPERACUTE (RARE – WITHIN MINUTES OF THE TRANSPLANT),
ACUTE (ONE TO THREE WEEKS AFTER) OR CHRONIC REJECTION (ANYTIME);
FEVER, FLULIKE SYMPTOMS, SHORTNESS OF BREATH, CHEST PAIN, WEIGHT
GAIN (2 LB IN 2 DAYS OR 5 LB IN ONE WEEK), FATIGUE, ELEVATED BLOOD
PRESSURE – NEED ENDOMYOCARDIAL BIOPSY (WKLY FOR 3-6 WKS, THEN Q
3 MONTHS FOR FIRST YEAR, THEN YEARLY UNLESS SYMPTOMATIC)
HEART TRANSPLANTATION
• CLINICAL SIGNS AND SYMPTOMS OF
REJECTION
• FEVER OVER 100 °F (38 °C)
• FLULIKE SYMPTOMS SUCH AS CHILLS,
ACHES, HEADACHES, DIZZINESS,
NAUSEA, AND VOMITING
HEART
TRANSPLANTATION
• SHORTNESS OF BREATH
• NEW CHEST TENDERNESS/PAIN
• WEIGHT GAIN OVER 2 LB FOR 2
DAYS IN A ROW, OR A TOTAL OF 5
LB IN A WEEK
• FATIGUE AND MALAISE
• ELEVATED BLOOD PRESSURE (BP)
HEART
TRANSPLANTATION
• IMMUNOSUPPRESSIVE DRUGS:
CYCLOSPORINE (SANDIMMUNE),
AZATHIOPRINE (IMURAN),
PREDNISONE (METICORTEN),
TACROLIMUS (PROGRAF), OR
MYCOPHENOLATE (CELLCEPT)
• DRUGS HELP PREVENT
REJECTION, SIDE EFFECTS
INCREASE THE RISK FOR
INFECTION, FLUID
RETENTION,
HYPERTENSION, AND
DIABETES
HEART
TRANSPLANTATION
• HIGH COST: PRE-HEART
TRANSPLANT
EVALUATION, SURGERY,
DRUGS, POST-SURGERY
CARE, AND FOLLOW-UP
TESTS APPROXIMATELY
ONE MILLION INSURANCE AND
MEDICARE OR MEDICAID
ASSUME MOST OF COST
HEART
TRANSPLANTATION
• INFECTION
• CAUSES: BACTERIAL, VIRAL, AND FUNGAL
INFECTIONS DUE TO IMMUNOSUPPRESSIVE
DRUGS; SYMPTOMS SIMILAR TO REJECTION
• LIFE THREATENING; TREATED WITH
ANTIBIOTICS, ANTIVIRALS, ANTIFUNGALS
HEART
TRANSPLANTATION
CARDIOVASCULAR DISEASE
TRANSPLANTED HEART BEATS FASTER THAN
NATURAL HEART, 100 TO 110 BEATS/MINUTE,
BECAUSE NERVES THAT AFFECT HEART RATE HAVE
BEEN SEVERED - CAD COMMON PROBLEM
AMONG HEART TRANSPLANT RECIPIENTS - DO
NOT EXPERIENCE ANGINA BECAUSE HEART’S
NERVE SUPPLY IS NOT INTACT
• RATE OF SURVIVAL: 85% TO 90% 1 YEAR
AFTER SURGERY, 10-YEAR SURVIVAL 56%
ORTHOTOPIC
TOTAL ARTIFICIAL HEART
– TAH
• TOTAL ARTIFICIAL HEART (TAH): ELECTRICALLY POWERED
PUMP THAT CIRCULATES BLOOD INTO THE PULMONARY
ARTERY AND THE AORTA
• REPLACING THE FUNCTIONS OF BOTH RIGHT AND
LEFT VENTRICLES
• TARGETED FOR THOSE WHO ARE UNLIKELY TO LIVE
MORE THAN A MONTH WITHOUT INTERVENTION
• CONSIDERED – BRIDGE TO TRANSPLANT OR TO
DESTINATION THERAPY