Cardiovascular
Disorders
GREAT WEB SITES FOR
ARRHYTHMIA RECOGNITION AT BOTTOM OF PAGE!
(Material taken from source textbook, Ignatavicius, Donna et al.
MEDICAL-SURGICAL NURSING ACROSS THE HEALTH CARE CONTINUUM, W.B.
Saunders Co., Philadelphia, Pa., 3rd. ed., 1999)
Valvular
Disorders:
1. Mitral
Stenosis: inhibition of normal blood
flow from left atrium to left ventricle due to valve leaflet
thickening and narrowing of valve orifice
Usually results from rheumatic
carditis
Back pressure into left atrium causes
pulmonary congestion, R ventricular hypertrophy and R heart failure
leading to L heart failure as preload falls and cardiac output(CO)
decreases
S & S= Dyspnea on exertion(D.O.E.),
orthopnea, PND(Paroxysmal Nocturnal Dyspnea), dry cough; eventually,
pulmonary edema, hemoptysis and R heart failure with JVD, peripheral
edema, hepatomegaly
Physical Exam reveals a rumbling, apical
diastolic murmur, irregularly, irregular pulse if atrial fibrillation
present--which is a common finding
2. Mitral Regurgitation or
Insufficiency: valve does not
close completely during systole due to valve
calcification
Rheumatic heart disease most common
etiology
Increased volumes and pressure in left
atrium and ventricle eventually cause dilation and hypertrophy of the
left chambers of the heart
S & S=fatigue, weakness r/t
decreased CO(Cardiac Output) as L ventricle decompensates; pt. c/o
palpitations, anxiety, atypical chest pain. L and R heart failure
develop
Physical Exam reveals high-pitched
Holosystolic murmur at the apex, with radiation to L axilla; pulse is
irregularly irregular with atrial fibrillation which is common.
Severe regurgitation often exhibits an S3 heart
sound.
3. Mitral Valve
Prolapse: valvular leaflets
enlarge and prolapse into the left atrium during systole; often
benign abnormality, but may progress to Mitral Valve
Regurgitation.
Familial tendency
S & S=palpitations, decreased
exercise tolerance, atypical chest pain, dizziness, syncope
associated with dysrhythmias{such as atrial or ventricular
tachycardia}
Physical Exam reveals midsystolic click
and late systolic murmur audible at apex
4. Aortic Stenosis:
valve narrows, preventing L
ventricular outflow during systole; this increased systemic vascular
resistance(SVR) leads to L ventricular hypertrophy. L sided heart
failure and eventually R occur:
Congenital malformations, rheumatic
carditis and atherosclerosis and degenerative calcification of the
aortic valve in the elderly
LVH(Left Ventricular Hypertrophy) and
fixed cardiac output(CO) eventually leads to L and R heart
failure
S & S=dyspnea, angina, syncope with
exertion
Physical Exam reveals narrow pulse
pressure and harsh, systolic crescendo-decrescendo murmur on
auscultation
5. Aortic
Regurgitation(Insufficiency):
valve does not close completely during diastole allowing
regurgitation of blood from the aorta back into the L ventricle. This
leads to LVH and L heart failure as in condition
above:
Cause may be infective
endocarditis(nonrheumatic), congenital malformation, hypertension, or
Marfan's Syndrome
May be asymptomatic for many
years
S & S= dyspnea, orthopnea, PND,
nocturnal angina with diaphoresis, palpitations which increase while
lying on L side
Physical Exam reveals a bounding pulse,
tachycardia, widened pulse pressure, and high-pitched, blowing,
decrescendo diastolic murmur on auscultation
Management: Depends on severity and
extent of accompanying cardiac
problems:
a. Nonsurgical
Treatments:
Prophylactic antibiotics before any
invasive procedure to prevent infective endocarditis
Rest
Drugs to treat heart failure(Digoxin or
diuretics) or atrial fibrillation(Cardizem and Digoxin) if this
develops; Coumadin must be prescribed for chronic atrial fib to
prevent embolic stroke.
Beta blockers are sometimes given for
troublesome palpitations or fast rates associated with mitral valve
prolapse; dysrhythmias may also need correction
b. Surgical Treatments:
Reparative Procedures include Balloon
Valvuloplasty for non-calcified, stenotic aortic and mitral valves
done through the femoral vein or artery without a surgical incision;
other reparative procedures are Direct or Open Commissurotomy for
stenosis and Mitral Valve Reconstruction for Mitral
Insufficiency--these require open heart surgery and cardiac
bypass.
Replacement of Valves also requires open
heart surgery and cardiac bypass. Two main types of replacements are
used: (1) Biological tissue valves(xenographs from pigs-->
"porcine" and (2) prosthetic valves made from various metals and
synthetic materials.
Biological valves only last 7 to 10
years, but do not require lifelong anticoagulation
Prosthetic valves(St. Jude or
Starr-Edwards) are very durable,but require lifelong anticoagulation
therapy
Pre and Postop care similar to patient
undergoing Coronary Artery Bypass Grafts(CABG)
Inflammations and
Infections
1. Infective Endocarditis(Bacterial
Endocarditis):
Occurs in I.V. drug users, pts. with
valve replacements or structural defects
Caused by vegetations on
valves
Ports of entry usually oral
cavity(dental work), skin, urinary or G.I. infections, surgery, I.V.
lines
S & S=fever, anorexia,wgt. loss,
cardiac murmur, heart failure, systemic embolization, petechiae,
splinter hemorrhages in nail beds, Osler's nodes on fingers, hands,
and toes,and Janeway's lesions on fingers, toes, nose or
earlobes
Diagnosed by positive blood cultures,
echocardiograms showing endocardial involvement and a new regurgitant
murmur
Interventions include rest, I.V.
antibiotics for 4 to 6 weeks or surgery for
complications
Teaching includes avoidance of
irrigation or flossing when brushing teeth, manifestations of
endocarditis and heart failure and when to call physician. Pts. must
remind health care providers to prescribe prophylactic antibiotics
before any invasive procedure.
2. Pericarditis:
Acute pericarditis--associated with
malignant neoplasms, infections, post M.I., post Cardiac Surgery,
Lupus
Chronic pericarditis--associated with
T.B., radiation therapy, trauma, end stage renal disease(ESRD), or
metastatic cancer
S & S=precordial pain radiating to L
neck, shoulder or back--worse when supine, relieved with sitting up
and forward and aggravated by inspiration, coughing or swallowing; a
precordial friction rub is heard at L lower sternal border. There may
be pleural effusion with acute pericarditis. Pts. with chronic
pericarditis may have R heart failure and atrial
fibrillation.
Diagnosed by blood cultures, CT scans,
echos, ekg changes
Treatment includes NSAIDS for pain
relief, antibiotics for infections, corticosteroids to relieve
inflammation if the cause is nonbacterial. Uremic pericarditis is
treated with hemodialysis. Surgery is done for chronic constrictive
pericarditis to remove the thickened membrane that forms. In acute,
sometimes a pericardial window must be done to drain excess fluid
from the pericardial sac.
Complications include pericardial
effusion leading to cardiac tamponade
CORONARY
ARTERY DISEASE
1. CONCEPTS BASIC TO UNDERSTANDING
CARDIAC FUNCTION (CHAPTER 35):
A. Coronary arteries anatomy (NAME THE
CORONARY ARTERIES AND THE AREAS OF THE HEART THAT THEY SUPPLY):
1. Left Main to Left Anterior Descending(LAD)--supplies
Anterior Wall and Septum
2. Right Coronary Artery(RCA)--supplies Inferior Wall, Sinus
node and AV node
3. Circumflex Coronary Artery(CCA)--supplies Posterior Wall,
Lateral Wall and Sinus and AV nodes
B. Terms: Cardiac Output (CO)= HR(HEART
RATE) X Stroke Volume
Cardiac Output--NORMAL VALUE IN
ADULTS?
Volume of Blood in liters/minute; normal is between
4-7L/min. in an adult
Cardiac Index--Normal Value in
Adults?
Based on Body Surface Area or the Size of the
patient--more accurate than Cardiac Output Formula
CI=CO ÷ BSA; 2.7 -3.2L/min./m2
Stroke Volume
The amount of blood ejected by the Left Ventricle with
each systole(contraction); the Four Determinants of Cardiac Output
are listed below:
1. Preload--degree of myocardial fiber
stretch at end of diastole just before contraction;
Starling's
Law--the more the heart is
stretched(within limits), the more forcefully it
contracts
(LVEDP--Left Ventricular End
Diastolic Pressure--relation to Preload?)
LVEDP= Preload
In pathological states: increased
preload in CHF and decreased preload in hypovolemic
shock
2. Afterload--The pressure or resistance
that the ventricles must overcome in order to eject blood through the
valves to the lungs and body; afterload depends on the Blood Pressure
and the diameter of the blood vessels.
Hypertension increases afterload.
3. Contractility (Contrast with
Cardiomyopathy)--the strength and force of myocardial
contraction--decreased in hypoxia, acidemia or heart damage;
Inotropics are drugs given to increase
contractility.
Ejection
Fraction(reflects contractility)--the
amount of blood the Left ventricle ejects with each
contraction--measured in %(determined through diagnostic tests such
as the Echocardiogram and Cardiac Cath)
Normal=65%(range=50-75%)
4. Heart Rate--compensates for a decreasing
CO by speeding up(sympathetic response), but this increases
myocardial oxygen demand
C. Diagnostic Testing:
Echocardiogram--measures and shows what? dx
of pericardial effusion, cardiomyopathy, valvular dysfunction;
identifies areas of hypokinesis of myocardium and determines ejection
fraction
Stress Test--types and purpose?
Exercise (Treadmill) or Chemical (heart
is stressed with drugs(Persantine, Dobutrex); a scan is done with
Thallium or Cardiolite(radioisotopes) to assess blood supply or lack
of it to areas of the heart muscle
Cardiac Catheterization--post care
considerations? Check vital signs on ordered schedule; check groin
for bleeding--use pressure dressing or M.D. uses "plug" ; check
distal pulses and keep affected leg straight
Difference between right and left
cath?
Right--catheter is passed up
vena cava to right side of heart through the femoral vein; pressures
of the chambers may be determined
Left--catheter is passed up
aorta via the femoral artery; pressures of the left side are
determined as well as ejection fraction, patency of coronaries
through injection of contrast media
Lecture
Outline:
1. ANGINA PECTORIS
A.
DEFINITION: Narrowing of coronary
arteries with resulting ischemia to the myocardium when O2
demand exceeds O2 supply ; Ischemia is
reversible, limited and does not cause permanent damage; chest pain
is relieved by rest and/or nitroglycerine
B. TYPES:
(1) STABLE--occurs with stress(exertion,
cold) in a predictable fashion and is relieved by rest and/or
nitroglycerine
(2) UNSTABLE(USA)--Chest pain occurs at
rest or with minimal exertion; there is an increase in frequency and
duration of pain, poorly relieved by rest or nitro; predictive of an
M.I. without intervention
Descriptive
Terms:
(a)
New-onset
(b)
Prinzmetal's
(c)
Preinfarction
(d)
Crescendo
(e)
Atypical
2. MYOCARDIAL INFARCTION
(MI)
A.
DEFINITION--Sudden deprivation of
O2 supply to the myocardium(>80-90% occlusion of
coronaries) resulting in ischemia leading to necrosis(infarction)
unless blood flow is quickly reestablished
B.
PATHO: "Time is
Muscle"--infarction is an evolving process over several hours. It
often begins with the subendocardial layer--"zone of
necrosis"--surrounded by the "zone of injury" and "zone of
ischemia"
"SUBENDOCARDIAL MI" OR "NON-Q WAVE
MI"--involves damage to first layer and has less effect on wall
motion and cardiac output than a transmural MI
"TRANSMURAL MI"--involves all three
layers of muscle; pathological Q waves are evident and remain on 12
Lead EKG forever; has an adverse effect on cardiac output and wall
motion
C. CLASSIFICATION BY
LOCATION: Signs and Symptoms of
MI depend on which coronary artery was obstructed and which part of
the ventricular wall was damaged
(1) AMI(Anterior MI supplied by
LAD)--25% of MIs; high risk of left ventricular failure and
dysrhythmias
(2) INFERIOR WALL MI(supplied by
RCA)--17% of MIs; risk of dysrhythmias resulting from sinus and AV
node dysfunction(bradycardia or heart blocks); also, one third of
patients have R ventricular failure
(3) POSTERIOR OR LATERAL WALL
MI(supplied by Circumflex)--3% of MIs; causes sinus and AV
dysrhythmias
D. RISK FACTORS:
(1) NON MODIFIABLE--age, sex, family hx,
ethnic background
(2) MODIFIABLE--hyperlipidemia, smoking,
HTN, impaired glucose tolerance, obesity, sedentary life style,
stress
E. DIAGNOSTIC STUDIES:
(1) CARDIAC
ENZYMES--CPK or CKMB--
isoenzymes that start to rise
within 3
hrs. after symptoms of MI, peak
12-24 hrs and return to normal within 48 to 72 hrs. Now there are
subforms of
CKMB(CkMB1 and
CkMB2) that start to rise within
1-2
hrs. after onset of
pain.
Troponin
1--rises within
4
hours of symptoms; very specific
for only myocardial muscle damage; also is predictor of
prognosis(higher elevations associated with a worse outcome); are
still detectable in blood for several weeks after MI
LDH
elevation--not used as much since
Troponin has become standard
The LDH isoenzyme "flip"--LDH1 becomes higher than
LDH2
(2) CBC--WBC elevated between 10-20,000
second day to one week following MI; slight elevation in temperature
is present with this inflammatory response
(3) 12 LEAD EKG--MI causes ST-T wave
changes in certain leads; Peaked T waves may be first sign, along
with ST elevation, T wave inversion, and eventual Q wave formation.
ST depression may be seen with ischemia.
(4) STRESS TEST--discussed above;
Exercise or Chemical stressors applied to heart
(5) SCANS--Thallium used with stress
test to assess areas of ischemia
(6) CARDIAC CATH--discussed above and
used to determine extent and types of blockages and what kind of
treatment should be done(CABG, PTCA, etc.)
F.
COMPLICATIONS: DYSRHYTHMIAS,
PULMONARY EDEMA, CARDIOGENIC SHOCK, HEART FAILURE, ANEURYSMS OF HEART
WALL WITH VENTRICULAR RUPTURE ; EXTENSION OF MI
G. MANAGEMENT:
GOALS: DECREASE MYOCARDIAL O2
DEMANDS WHILE INCREASING MYOCARDIAL O2
SUPPLY
(1) INITIAL OR EMERGENCY(CHEST
PAIN CENTER):
THE CHEST PAIN CENTER IS A SPECIAL AREA IN THE ER FOR CLOSE
MONITORING AND INTERVENTIONS FOR PATIENTS HIGHLY SUSPICIOUS OF HAVING
AN MI; THE PRINCIPLE IS TO DIAGNOSE ASAP IN ORDER TO INSTIGATE
MEASURES TO REPERFUSE THE MYOCARDIUM TO LIMIT OR PREVENT PERMANENT
DAMAGE.
"TIME IS
MUSCLE"
THROMBOLYTIC THERAPY SHOULD BE INITIATED
ASAP UP TO A LIMIT OF SIX HOURS FOR MAXIMUM BENEFIT FOR SUITABLE
CANDIDATES WHO HAVE NO CONTRAINDICATIONS OR THE M.D. MAY DECIDE TO DO
AN EMERGENCY CATH AND PROCEED FROM THERE TO AN ANGIOPLASTY OR CABG
DEPENDING ON FINDINGS.
PATIENTS IN THESE CHEST PAIN CENTERS HAVE
SPECIAL CARDIAC MONITORING AND TRAINED PERSONNEL THAT CAN CONFIRM AN
EVOLVING MI BY ST-T WAVE CHANGES, ELEVATIONS OF CARDIAC SPECIFIC
ENZYMES, SIGNS AND SYMPTOMS AND HISTORY OF PRESENT
ILLNESS.
GENERALLY, ASA IS GIVEN AS WELL AS O2
THERAPY ALONG WITH A NITRO DRIP FOR PAIN CONTROL AND VASODILATION OF
THE CORONARIES.
(2)
DRUGS:
a.
Thrombolytics--given
within six hours for maximum benefit, the earlier the better.
Generally, chest pain unrelieved by nitro within 30 minutes, with
evidence of transmural ischemia or injury evident on the EKG, and
with no contraindications is the criteria for administration of
Thrombolytics like Activase,
Reteplase, or TNKase followed by
a Heparin drip and/or an antiplatelet medication.
b.
Anticoagulants--Heparin
drip, eventually Coumadin therapy --please review lab tests that
monitor therapy
c.
Antiplatelet
Agents--ASA immediately, Ticlid,
Plavix later. An I.V. agent may be given like
Aggrastat(Tirofiban).
d.
Oxygen--given
to increase myocardial supply, usually 2-4 liters/nc unless patient
is critical and needs intubation and mechanical ventilation because
they come in after a cardiac arrest or have developed acute pulmonary
edema or cardiogenic shock.
e.
Morphine
Sulfate--a vasodilator to relieve
pain , anxiety and decrease preload, reduce pulmonary edema and
reduce myocardial oxygen demands
f.
Nitrates--Given
I.V. titrated to control chest pain, reduce preload and afterload,
and dilate the coronary arteries. This drug also reduces myocardial
oxygen demands. Blood Pressure must be monitored
continuously.
g.
Beta
Blockers--These drugs are given
to decrease infarction size, reduce ventricular dysrhythmias, prolong
the period of diastole in the cardiac cycle so that increased blood
flow will be delivered to the myocardium through the coronaries; the
force of the myocardial contractions is also reduced. Research has
shown that there are improved survival rates when these drugs are
given. Heart rate and blood pressure must be carefully
monitored.
h.
Calcium Channel
Blockers--Various Calcium Channel
Blockers are given after an MI, for example, Cardizem is given as a
drip to convert atrial fibrillation; Verapamil may be given I.V. for
SVT(Superventricular Tachycardia). These drugs are given to dilate
the coronary arteries and reduce vasospasm. Again, check heart rate
and blood pressure carefully.
i.
Ace
Inhibitors--Given to reduce
afterload and prevent heart failure post MI.
j.
Inotropics or
Sympathomimetics:(All the
following should be given through a central line and have the
potential to cause ventricular dysrhythmias)
Dobutamine(Dobutrex)--stimulates
Beta 1 receptors in cardiac muscle to increase contractility and
improve stroke volume
Milrinone(Primacor)--increases
contractility and increases left ventricular function
Dopamine(Intropin)--given
to increase contractility at the dose of 5-10mcg/kg/min.; given to
increase Blood Pressure at the dose of 10-20mcg/kg/min. for
shock
(3) PROCEDURES in Cath
Lab:
a. PTCA (Percutaneous Transluminal
Coronary Angioplasty)--can be done to open obstructed areas in the
coronaries if there is only single or double vessel disease with
discrete, proximal, noncalcified lesions.
b. Rotoblader-- called an
"Arthrectomy"--removal of calcified plaque with a diamond tipped
device; procedure similar to PTCA.
c. Stenting--done with angioplasty to
prevent restenosis of the coronary artery; the placement of one or
more stents maintains a patent lumen; antiplatelet drugs are given
after the procedure and on discharge.
H. NURSING
CARE: Use Text to help complete
the following:
(1) ASSESSMENT--Describe the typical
chest pain associated with an MI. Atypical?
(2) NURSING DIAGNOSIS--What are the
priorities?
(3) INTERVENTIONS: "Standing
Orders"Orders that cover every patient admitted
PCU/CCU
a. Chest pain Management
b. Dysrhythmia recognition and
management
c. Preparation for tests
d. Post test care
Cardiac Cath? Review--
e. Drug Therapy
monitoring
f. Positioning, Rest &
Activity
g. Psychological Care
h. Diet Therapy
i. Teaching
j. Cardiac
Rehabilitation:
PHASE I--instituted during the hospital
stay until discharge; education given about CAD, modifying risk
factors, smoking cessation, rest vs. activity
PHASE 2--Discharge through convalescence
at home with supervised outpatient exercise program to achieve
improved physical and cardiac conditioning
PHASE 3--long term
conditioning
Site for help with cardiac disorders: http://www.acc.org(American
College of Cardiology) or:
Site for Heart Surgery:
or