CARE OF CLIENTS WITH CARDIOVASCULAR DISORDERS

By: Jerald S. Ugdoracion MN- MSN

atrial diastole and

ASSESSMENT OF CLIENTS WITH ventricular systole)
CARDIOVASCULAR DISORDERS ii. S2 – “dub” sound : closure
• Nursing History of the Pulmonic and
o Modifiable Factors Aortic Semilunar valves
o Non –Modifiable Risk Factors (onset of ventricular
diastole)
• Physical Examination iii. S3 – abnormal sound also
• Common Clinical Manifestations known as Ventricular
diastolic gallop in older
• Diagnostic Examinations
adults but is considered
normal among children
NURSING HISTORY:
and young adults
iv. S4 – common in
A. MODIFIABLE RISK FACTORS
Congestive Heart Failure
a. Stress
also known as Atrial
b. Diet
diastolic gallop
c. Exercise
d. Cigarette Smoking
b. Murmurs
e. Alcohol intake
c. Pericardial friction Rub – sound
f. Hyperlipidemia
originating from pericardial Sac.
g. Other disorders (e.g. Obesity,
Short, high-pitched and scratchy
Diabetes Mellitus)
sound usually showing sign of
h. Personality Type and Behavioral
inflammation, infection or
factors
infiltration.
i. Use of Contraceptive Pills

B. NON-MODIFIABLE FACTORS
COMMON CLINICAL MANIFESTATIONS
a. Age
b. Gender
a. Dyspnea (shortness of breath)
c. Race
d. Heredity • Dyspnea on exertion
• Orthopnea
PHYSICAL EXAMINATION • Paroxysmal Nocturnal Dyspnea
b. Chest Pain
A. INSPECTION c. Edema
a. Skin color d. Syncope
b. Neck Vein distention e. Palpitations – characterized as
c. Respiration “pounding”, “racing” or “skipping”
d. Point of Maximal Impulse (PMI) heartbeats
e. Peripheral Edema f. Fatigue

B. PALPATION
a. Peripheral Pulses DISORDERS OF THE CARDIOVASCULAR
b. ApicalPulse SYSTEM

C. AUSCULTATION A. Inflammatory Disorders

a. Heart Sounds a. Rheumatic Fever
i. S1 – “lub” sound : closure b. Endocarditis
of the Mitral valves and c. Pericarditis
Tricuspid valves (onset of d. Myocarditis
B. Deficiency in Blood Supply to Myocardium
 a. Angina Pectoris • weakness and shortness of breath
b. Coronary Artery Disease (CAD) /
Coronary Atherosclerotic Heart Complications: Myocarditis, Endocarditis,
Disease (CAHD) Pericarditis, Pancarditis, Valvular defects,
c. Myocardial Infarction Congestive Heart Failure
C. Cardiac Arrythmias
a. Sinus arrhythmias
Diagnostics:
b. Atrial Arrythmias
c. Ventricular Arrythmias
d. Conduction defects / Heart Blocks / • The Jones criteria require the presence of 2
AV Blocks major or 1 major and 2 minor criteria for the
D. Mitral Valve Defects diagnosis of rheumatic fever.
a. Mitral Stenosis o The major diagnostic criteria
b. Mitral Insufficiency include carditis, polyarthritis,
c. Aortic Stenosis chorea, subcutaneous nodules, and
d. Aortic Insufficiency erythema marginatum.
e. Tricuspid Insufficiency o The minor diagnostic criteria
E. Congestive Heart Failure include fever, arthralgia, prolonged
F. Peripheral Vascular Disease PR interval on ECG, elevated acute
a. Thromboangitis Obliterans phase reactants (increased
b. Arteriosclerosis Obliterans erythrocyte sedimentation rate
c. Reynaud’s Disease [ESR]), presence of C-reactive
d. Thrombophlebitis protein, and leukocytosis.
e. Varicose Veins • Additional evidence of previous group A
streptococcal pharyngitis is required to
diagnose rheumatic fever. One of the
following must be present:
INFLAMMATORY DISORDERS o Positive throat culture or rapid
streptococcal antigen test result
o Elevated or rising streptococcal
antibody titer
o History of previous rheumatic fever
RHEUMATIC HEART DISEASE or rheumatic heart disease
o Increased ESR, WBC count and C
A disease condition characterized by damage to the reactive protein
heart and its membranes brought about by
complications of rheumatic fever. It is common
Medical Management:
among children between 5 and 15 years old and is
rare among adults. It is caused by Group A
Streptococcal Infections and is believed to be caused Medical therapy in rheumatic heart disease is directed
by antibody cross reactivity. Scarring of the heart toward eliminating the group A streptococcal
valves may occur leading to additional workload for pharyngitis (if still present), suppressing
the heart. inflammation from the autoimmune response, and
providing supportive treatment for congestive heart
Clinical Manifestations: failure.

• fever 1. Antimicrobial therapy

a. Long term narrow spectrum
• swollen, tender, red and extremely painful
cephalosphorins, amoxicillin-
joints - particularly the knees, ankles,
clavulanate, oral clindamycin,
elbows, or wrists
dicloxacillin, penicillin,
• nodules over swollen joints
erythromycin and other macrolides.
• red, raised, lattice-like rash, usually on the Erythromycin Estolate is given
chest, back, and abdomen when clients are allergic to
• uncontrolled movements of arms, legs, or Penicillin
facial muscles
 2. Salicylates and Steroids for pain control and
fever (e.g. Prednisone, Aspirin)
3. Digoxin, Diuretics (Furosemide and
Spironolactone) and Supplemental O2 is
given among clients who developed
congestive heart failure after RHD.
i. Check Potassium levels of
patient prior to initiating
digoxin therapy to prevent
possibility of toxicity
ii. Loading dose : 1.25-1.5
mg/d Maintenance dose:
0.25-0.5 mg/d
Therapeauic Level: 1.5-2
ng/ml
4. Rest – to maintain optimum cardiac function
5. Prevention of Recurrent episodes by Long
term use of penicillin (Penicillin G 0.6 to 1.2
million units injections every 4 weeks for 5
years or until age 21 for patients with RHD
without carditis but for 10 years or until age
40 for patients with RHD with carditis.
6. Surgical Management is only indicated
when severe valvular damage has already
occurred to the heart that cardiac functioning
has already been impaired.
Nursing Interventions:
A. Reducing Fever
a. Administer penicillin therapy or
erythromycin therapy when allergic
to penicillin
b. Give salicylates as prescribed
c. Tae and record temperature every 3
hours and evaluate comfort level of
patient for evaluation of drug
effectivity
B. Maintaining Adequate Cardiac Output
a. Assess for complains of chest pain,
palpitations or precordial tightness,
tachycardia as this may indicate
development of carditis
b. Auscultate for murmurs or
pericardial friction rub
c. Monitor the development of
chronic rheumatic endocarditis
whichmay include valvular
disorders leading to CHF.
C. Maintaining Activity
a. Maintain bedrest if fever persists or
if signs of carditis are present
b. Provide active-assistive ROM
programs
c.Provide diversional activities that
prevents exertion
D. Patient Education
a. Counsel the patient on hygienic
practices
b. Counsel on the importance of
adequate nutrition and rest periods
c. If sore throat occurs, tell patient to
immediately seek medical
consultation
INFECTIVE ENDOCARDITIS
An infection on the valves and the endothelial surface
of the heart brought about by bacterial invasion that
may progress to deformities of the cardiac valves and
cardiac insufficiency.
Common Affecting Microorganisms:
Streptococci, Pneumococci and Staphylococci, Fungi
and Rickettsiae
Other Risk Factors:
a. Disorders on the valves of the
heart
b. Age : more common among
older people
c. Intravenous drug use
d. Hospitalization : occurs
commonly among patients
with debilitating disorders that
requires indwelling catheters
or prolonged IV access
e. Immunosuppression : Fungal
Endocarditis
Complications: Valvular defects, heart failure,
embolism and poor perfusion to various
organs.
Clinical Manifestations:
a. General manifestations of malaise,
anorexia, weight loss and intermittent fever.
b. Roth’s Spots : hemorrhages with pale
centers in fundi of eyes
c. Osler’s Nodes : nodules that are small and
painful in pads of fingers or toes
d. Cardiac Manifestations: heart
enlargement, heart failure, heart murmurs
e. Varied manifestations according to areas
of embolism (e.g. Myocardial
Ischemia on heart, stroke on brain,
hematuria and renal failure on kidney)
Diagnostics:
a. Serial Blood Culture and
Sensitivity
Medical Management:
a. Adequate dosages of Antimicrobial
Agents depending on Causative Agent
(continuous IV infusion for 2-6 weeks)
b. Seriously damaged valves may
require surgical intervention: Surgical
Valve Replacement
Nursing Management:
a. Provide psychosocial support
b. Provide post surgical care to clients if
patient received surgical intervention
c. Monitor patient’s temperature : Fever may
be present for weeks
d. Monitor for signs of Systemic Embolization
or poor organ perfusion
e. Instruct patient and family about activity
restrictions and signs and symptoms of
infection
f. Reinforce that antibiotic prophylaxis is
recommended for patient who had previous
Endocarditis and who are to be subjected
with invasive procedures
g. Refer to home care nurse to supervise and
monitor intravenous antibiotics
PERICARDITIS
Inflammation of the pericardium , the membranous
sac enveloping the heart. Usually caused by viral
infection but may be caused by bacteria and fungi at
times.
Can be classified by what accumulates in the
pericardium:
a. Serum : Serous
b. Pus : Purulent
c. Calcium deposits : Calcific
d. Clotting Proteins : Fibrinous
e. Blood : Sanguinous
Complications: Pericardial Effusion, Cardiac
Tamponade
Picture Illustrating
Cardiac Tamponade
Clinical Manifestations:
a. Pain felt beneath the clavicle and in the
neck and left scapular region,
aggravated by breathing, turning in bed
and twisting of body and is relieved by
leaning forward or sitting up (Friction
rub)
b. Dyspnea
c. Fever, High WBC count
Cardiac Tamponade Clinical Manifestations:
a. Falling BP, rising venous pressure
(distended neck veins), and distant
(muffled) heart sounds with pulsus
paradoxus
b. Anxiousness, confusion and restlessness
c. Dyspnea, Tachypnea and Precordial
Pain
d. Elevated CVP
Medical Management:
a. Bed Rest is instituted when patient’s cardiac
output is severely impaired
b. Pharmacologic Therapy:
a. Narcotic analgesics for Pain relief
during the acute phase
b. Analgesic and NSAIDS to hasten
reabsorption of fluid in the
pericardial sac ; Colchicine may be
an alternative medication
c. Corticosteroids
d. Penicillin : DOC if pericarditis is
due to rheumatic fever
e. Isoniazid, Rifampicin,
Pyrazinamide, Ethambutol and
Streptomycin if pericarditis is
caused by tuberculosis
f. Amphotericin B if caused by fungal
infection
c. Surgical Management
a. Pericardiocentesis : removal of
pericardial fluid
b. Pericardiectomy : removal of the
tough encasing pericardium
Nursing Management:
a. Assess pain and possible presence of
precordial pain.
b. Monitor temperature frequently
c. Assess for presence of pericardial
friction rub. Differentiate Pericardial
Friction rub from Pleural Friction Rub
 (audible upon auscultation and
synchronous with heartbeat and is
continuous)
d. Advise bed rest or chair rest in sitting
upright or leaning forward position
e. Instruct patient to resume ADLs
gradually as tolerated when pain and
friction rub abate and to resume bedrest
when pain and friction rub recur
f. Monitor for triad manifestation of
Cardiac Tamponade : (1) Falling arterial
pressure (2) Rising venous pressure (3)
Distant heart Sounds. Report
immediately if present to prevent
cardiac tamponade and prepare for
pericardiocentesis
MYOCARDITIS
An inflammatory process that involves the
myocardium which results from an infectious process
(e.g. viral, bacterial, mycotic, parasitic, or protozoal)
that may threaten life due to progressive myocardial
degeneration.
Clinical Manifestations:
a. Fatigue, Dyspnea, Palpitations and
occasional discomfort in the chest
orupper abdomen
b. Pericardial Friction rub if accompanied
with pericarditis
c. Fever
d. Pulsus alternans may be present
Complication: Heart Failure
Assessment and Diagnostics:
a. Cardiac enlargement as revealed by
cardiac roentgenography
b. Faint heart sounds upon auscultation
c. Gallops and murmurs may be present
d. Confirmatory diagnostic procedure :
ENDOMYOCARDIAL BIOPSY
Medical Management:
a. Bed rest to decrease cardiac workload
b. Continuous cardiac monitoring to detect
possible dysrythmias
c. Digitalis use: to decrease the heart rate
while improving contractility of the
heart
Nursing Management:
a. Monitor for digitalis toxicity for clients
who are receiving digitalis therapy :
Nausea, Anorexia, Vomiting, Diarrhea,
Bradycarda and Blurring of Vision
b. Instruct patient to increase physical
activity when tolerated and to report
any symptom that occur with increased
activity
c. Avoid competitive sports and alcohol
DEFICIENCY IN BLOOD SUPPLY TO THE
HEART
CORONARY ARTERY DISEASE (CAD) /
CORONARY ATHEROSCLEROTIC HEART
DISEASE (CAHD)
A condition characterized by abnormal accumulation
of lipid or fatty substances and fibrous tissues in the
myocardial vessel wall reducing the blood flow to the
myocardium. This is a progressive disease but can be
curtailed and in some case reversed.
If not prevented then this can lead to Myocardial
Infarction and Heart Failure
Modifiable Risk factors:
a. Cigarette Smoking
b. Elevated Blood Pressure
c. High Blood Cholesterol
(Hyperlipidemia)
d. Obesity
e. Diabetes Mellitus
f. Physical Inactivity
g. Use of Oral Contraceptives
h. Behavior patterns
Non-Modifiable Factors:
a. Positive Familial History : common among
people with 1st degree relatives who suffered
from cardiac disorders before age 50
b. Age : common among men more than 45
years old and women more than 55 years old
c. Gender : occurs 3 times more in men than in
women
d. Race: higher incidence among African
Americans
Clinical Manifestations:
a. Chest Pain (Angina Pectoris)
 b. Atypical symptoms of myocardial ischemia
(shortness of breath, nausea and unusual
fatigue)
c. Myocardial Infarction
Medical Management:
a. The goal of medical management is to
decrease cardiac oxygen demand and
increase O2 supply
b. Pharmacologic Therapy is instituted
especially if angina pectoris accompany
CAD:
• Fast Acting Nitrates (e.g.
Nitroglycerine)
Action: Causes peripheral
vasodilation resulting to a
decreased peripheral vascular
resistance decreasing blood
pressure and cardiac workload
Special Nursing Considerations:
a. Perform interventions that would
prevent complications of
Orthostatic Hypotension
b. Remember that fast acting nitrates
is the drug of choice for angina
pectoris; take a maximum of three
doses given in 5 minute interval. If
not effective rush client to hospital
c. Store nitroglycerine in cool, dark
places and change every 6 months
d. Sublingual nitroglycerine is the
fastest but may cause burning and
tingling sensation under the tongue
e. If using transdermal patches,
replace daily, wipe off before
replacement and rotate sites.
Remove prior to defibrillation to
avoid burns.
f. Observe for common signs of drug
effectivity – faintness, flushed
appearance, dizziness, headache :
Do not discontinue the drug
• Beta Adrenergic Blockers
i. Propanolol (Inderal)
ii. Metoprolol (Lopressor)
iii. Nadolol (Cogard)
iv. Atenolol (Tenormin)
v. Pindolol (Visken)
Action: Blocks the beta
adrenergic sites of the heart
preventing epinephrine from
performing its sympathetic
effects on the heart
Special Nursing
Considerations:
a. Avoid giving Non-
Selective Beta Blockers
(Propanolol) to clients
with impaired breathing
pattern or with labored
breathing. May cause
further respiratory
depression.
b. Adjust dosages of
Insulin to diabetics.
Propanolol can cause
hypoglycemia
• Anti-coagulants and Anti-platelet
Aggregation agents
o Heparin and Warfarin
o Ticlopidine, Aspirin,
Dipyridamole
Action: Prevents the formation
of clots by preventing the
blood clotting cascade
Special Nursing
Responsibilities:
a. Assess for signs and
symptoms of bleeding
b. Avoid straining on
defecation
c. Monitor PT levels
(Coumadin therapy) and
PTT levels (Heparin
therapy)
d. Keep antidotes ready :
Protamine Sulfate for
Heparin and Vitamin K
for Coumadin therapy
e. Minimize vegetables in
the diet to decrease
extraneous sources of
Vitamin K
• Calcium-Channel Blockers
o Verapamil
o Nifidipine
o Diltiazem
Action: Blocks the influx of
calcium in to the myocardium
decreasing the action potential
of the heart muscles
Special Nursing
Considerations:
a. Assess heart rate and BP
b. Monitor hepatic and renal
function
 c. Administer 1 hr before or
2 hrs after meals. Food
delays the absorption of
the medication
c. Surgical Management:
a. Percutaneous Transluminal
Coronary Angioplasty (PTCA)
i. Mechanical dilation of the
coronary vessel wall by compressing
the atheromatous plaque
ii. Recommended to clients
with single vessel coronary artery
disease
iii. A specially designed
balloon tipped catheter is inserted
under fluoroscopic guidance and
advanced to the site of coronary
obstruction
Special Nursing Considerations:
• Prior to the operation, an IV line is
inserted to the client
• Client is placed on NPO 8 hours
prior to surgery and preoperative
sedative and medications are given
• Inform client that surgery may take
30 minutes to 1 hour
• Inform client that a feeling of
pressure may be felt upon insertion
of the catheter and a flushing
feeling may be felt when
fluoroscopic dye is inserted
• Postoperatively, take the client to
the ICU for close cardiac
monitoring
• Check for bleeding on femoral site
and apply pressure bandage
Please refer to this internet website for
additional information:
http://www.youtube.com/watch?
v=N7nghr9TpSU&feature=fvw
b. Intravascular Stenting
i. Biologic stent is produced
through coagulation of collagen,
elastin and other tissues in the vessel
wall by laser, photocoagulation or
radio frequency- induced heat
ii. Prosthetic intravascular
cylindric stents maintain good
luminal geometry after balloon
deflation and withdrawal
c. Coronary Artery Bypass Graft
(CABG)
i. Recommended if more
than one branch of coronary artery is
narrowed by atheromatous plaques
ii. Main Purpose :
Myocardial revascularization
iii. Internal Mammary Artery
and Saphenous Vein : Most
commonly used grafts
Special Nursing Considerations:
• Prior to the operation, an IV line is
inserted to the client
• Client is placed on General
Anesthesia
• Postoperatively, take the client to
the ICU for close cardiac
monitoring
• Monitor pacing wires and breathing
and drainage tubes
• Monitors and tubes removed over
the next few days
Please refer to this internet website for
additional information:
http://www.youtube.com/watch?
v=MDKa1Do1lSU&feature=related
Nursing Management:
a. prevention of the development of CAD is
the focus
a. Daily management of Hypertension
: Instruct to take medication at
regular basis and never to stop
unless told by prescriber
b. Smoking cessation
c. Avoid passive smoking
d. Plan a regular exercise under
medical supervision
e. Follow a healthy heart diet : Low
Sodium and Low Fat Diet
f. Reduce stress
g. Allow adequate time for rest and
relaxation
ANGINA PECTORIS
A transient chest pain caused by insufficient blood
flow to the myocardium resulting in to myocardial
ischemia. It results when myocardial oxygen demand
exceeds myocardial oxygen supply.
Clinical manifestations:
 a. transient, paroxysmal substernal
precordial pain
b. heaviness or tightness of the chest that
radiates down to one or both arms, left
shoulder, jaw or neck and back
c. Pain relieved by NITROGLYCERINE
d. Pallor, diaphoresis, dyspnea, faintness,
palpitations, dizziness
Types of Angina Pectoris:
a. Stable Angina
o Chest pain lasts for less than 10-15
minutes and recurrence is less
frequent
b. Unstable Angina (Preinfarction Angina,
Cresendo Angina, Intermittent
Coronary Syndrome)
o Chest pain lasts more than 15
minutes but less than 30minutes
and recurrence is more frequent
while intensity increases
c. Variant Angina (Prinzmetal’a Angina)
o Chest pain may last longer than that
of unstable angina and may even
occur at rest
o Attacks tend to occur at the early
hours of the day
d. Nocturnal Angina
o Occurs only during at night and is
highly associated with rapid eye
movement (REM) sleep
e. Angina Decubitus
o Paroxysmal chest pain that occurs
when the client sits or stands up
f. Intractable Anina
o Chronic incapacitating angina
unresponsive to intervention
g. Postinfarction Angina
o Occurs after MI, when residual
ischemia may cause episodes of
anigina.
Precipitating Events of Angina Pectoris:
a. Exertion : too much exertion or
exercise done in a sporadic
manner
b. Emotions : Excitement (e.g.
sexual activity)
c. Eating a very heavy meal
d. Environment : Exposure to
very cold temperature
Collaborative Management:
a. Pharmacologic Therapy (similar to that
of CAD, pls refer to Pharmacologic
therapy for CAD)
b. Surgical Management (similar to that of
CAD, pls refer to Surgical
management for CAD)
Nursing Management:
a. Improve diet of the client. Change to
low sodium, low fat and high fiber diet
b. Improve activity of client according to
what is tolerable to the client
c. Promote comfort
d. Promote and improve tissue perfusion
e. Instruct patient to stop activity
immediately when symptoms manifest
f. Advise client to reduce emotional
outbursts, worry and tension
MYOCARDIAL INFARCTION
The formation of localized necrotic areas within the
myocardium. Follows suddenly from abrupt cessation
of blood and oxygen flow to the heart muscle.
Prolonged ischemia lasting for more than 35 minutes
can cause irreversible cellular damage and necrosis of
the myocardium. Alterations in function depends on
the size and location of an infarct
(for psychopathophysiology of Myocardial Infarction please see
Appendix A)
Classifications of Infarct:
a. Transmural Infarct
• Damage extends from endocardium
to epicardium
b. Subendocardial Infarct
• Affects the endocardial muscles
only
c. Intramural Infarct
• Seen in patchy areas of the
myocardium and is usually
associated with longstanding
angina pectoris
Three Areas that Develop in Myocardial
Infarction
a. Zone of Infarction
• Records pathologic Q waves in the
ECG
 • Irreversible damage, death to the
heart muscle due to extensive and
complete oxygen deprivation
b. Zone of Injury
• Records elevated ST segment
• Area of the heart muscle
surrounding the area of necrosis,
inflamed and injured, but still
viable of adequate oxygenation is
restored
c. Zone of Ischemia
• Records inversion of T-wave
• Surrounds the area of injury,
ischemic and viable
Clinical Manifestations:
a. Pain
• Crushing, severe, prolonged
unrelieved by rest or
nitroglycerine; often radiating
to one or both arms, the neck
and the back.
• Characterized by Levine’s sign
b. Anxiety and Apprehension
• Feeling of doom and
restlessness
c. Oliguria
• Urine flow less than 30 cc/hr
d. Fever
• Slight elevation of temperature
occurs within 24 hours and
extends 3 to 7 days
accompanied by leukocytosis
and elevated ESR
e. Indigestion
• “Gas pains around the heart”
nausea and vomiting
f. Acute Pulmonary Edema
• Sense of suffocation, dyspnea,
orthopnea, gurgling/bubbling
respiration
g. ECG changes
• MI causes elevation of ST
segment, Inversion of T wave
and enlargement of Q wave
h. Elevated CK-MB, Elevated LDH
and Elevated AST
• These cardiac enzmes are
produced abnormally high
because of cellular damage and
death
• Rise of CK-MB is the most
definitive findings in MI,
especially in the presence of
elevated LDH levels
i. Shock
• Systolic blood pressure below
80 mmHg, lethargy, cold,
diaphoresis, peripheral
cyanosis,
tachycardia/bradycardia, weak
pulse
Diagnostics:
a. Electrocardiogram
• MI causes elevation of ST
segment, Inversion of T wave
and enlargement of Q wave
b. Cardiac Enzyme Studies
a. Aspartate Aminotransferase (AST)
NL: 7-40 mu/mL
• Formerly known as SGOT,
elevated levels indicate tissue
necrosis
• Range with Myocardial
Infarction:
o Initial Elevation : 4- 6
hrs
o Peaks : 24-36 hrs
o Returns to normal : 4-
7 days
b. Creatine Phosphokinase (Ck-MB)
• It is the most specific cardiac
enzyme and is an accurate
indicator of Myocardial
damage
• Normal range: Males : 50-325
mu/ml Females: 50-250
mu/mL
• Range with Myocardial
Infarction
o Onset: 3-6 hrs
o Peaks: 12-18 hrs
o Returns to normal: 3-
4 days
c. Lactic Dehydrogenase (LDH)
• LDH1 is the most sensitive
indicator of myocardial
damage
• In MI : LDH 1 is elevated and
its level exceeds LDH 2. LDH
1/LDH2 ratio becomes flipped
• Normal range: 100-225 mu/mL
• Range in Myocardial
Infarction:
o Onset: 12 hours
 o Peaks : 48 hours
o Returns to Normal:
10-14 days
d. Troponin I and T
• Protein components
found on striated
muscles specific to the
heart
• Troponin T (84%
sensitivity o MI)
Troponin I (90 %
sensitivity toMI)
• Range in Myocardial
infarction:
• Onset: 3-6 hours
• Peak: 20 hrs
• Lasts longer than that of
Ck-MB
Complications:
Complications include arrhythmia, cardiogenic
shock, heart failure, pulmonary edema, cerebral or
pulmonary emboli, myocardial rupture, pericarditis,
postmyocardial infarction syndrome, and sudden
death.
Collaborative Management:
A. Pharmacologic Therapy
a. Analgesics
i. For pain relief. Important
because pain can cause
shock.
ii. DOC: Morphine Sulfate,
Lidocaine or
Nitroglycerine
administered IV
b. Thrombolytic Therapy
i. DOC: Streptokinase,
Urokinase, and TPA
(Tissue Plasminogen
Activators)
ii. Administered between 3-6
hours after the initial
infarction has occurred
iii. Given in order to lyse
blood clots that may have
occluded one of the major
arteries supplying blood
and oxygen to the heart
causing the infarction
iv. Nursing responsibilities
include monitoring the
client for bleeding and
assessment of neurologic
status
c. Anticoagulant Therapy
i. Administered after
thrombolytic therapy to
maintain patency of
coronary arteries
ii. Examples : Heparin and
Coumadin
d. Other Antihypertensives
i. Beta-Adrenergic Blockers
ii. Calcium Channel Blockers
iii. Angiotensin Receptor
Blockers
B. Treatment
a. Goals:
i. Prevention of further
tissue damage and
limitation of infarct size
ii. Maximize myocardial
tissue perfusion and
reduce myocardial tissue
demands
b. Supplemental Oxygen by Nasal
Cannula
c. Cardiac Monitoring to monitor
development of dysrhythmias
d. PTCA may be done to reopen
occluded arteries
e. Diet: Low sodium Low fat diet
f. Activity: Bed Rest is usually
prescribed for 24-48 hours to
decrease oxygen demand.
Progressive ambulation is
implemented as soon as possible,
unless complications occur.
CARDIOPULMONARY RESUSCITATION
(CPR)
Indicated during cardiopulmonary arrest
(breathlessness, pulselessness or clinical death) and is
instituted within 4-6minutes after the arrest to prevent
brain damage.
Two Types of CPR:
a. BLS – Basic Life Support
• involves the use of
hands, mouth and the sincere
desire to give a person a
second chance of life
b. ACLS – Advanced Cardiac Life
Support
• Involves BLS and the
use of equipments,
 emergency drugs and
fluids to monitor the
client and stabilize his
condition
CPR involves the ABCD of life support:
A – Airway
B – Breathing
C – Circulation
D – Definitive treatments
TECHNIQUES OF BASIC LIFE SUPPORT
Step 1: Assess LEVEL OF CONSCIOUSNESS
• Shake the victim’s
shoulders and asl “Are you ok?”
• If no response, place the
client in a Supine position on a firm surface
Step 2: Open the AIRWAY
• The tongue is the most common cause of
airway obstruction in an unconscious person
• Use the HEAD TILT-CHIN LIFT
MANEUVER and the JAW THRUST
methods for opening and maintaining airway
• Jaw thrust is recommended for clients with
suspended neck injury
• Take 3 to 5 seconds to look , listen and feel
for spontaneous breathing
A B
Picture A – Jaw Thrust Maneuver
Picture B – Head Tilt Chin Lift Maneuver
Step 3: Initiate ARTIFICIAL VENTILATION
• Give 2 initial breaths lasting for 1 ½ to 2
seconds. Watch for rise and fall of the chest
upon introduction of air. If no rise and fall
occurs, consider airway obstruction
Step 4: Assess CIRCULATION
• Check the carotid pulse (adult) for 5-10
seconds, brachial pulse for infant and child
• If no pulse, cardiac compression is initiated
Step 5: Initiate External Cardiac Compressions
• Place the heel of one hand on the area of 2
fingerbreadths from the xiphoid process
(adult); midsternum of the infant
• Depress the sternum with heels of both
hands (dominant hand over non-dominant
hand) 1 ½ - 2 inches for adults, heel of one
hand 1 ½ - 2 inches for children and 2
fingers ½ - 1 inch for infant
• If 2 rescuers: 80-100 compressions per
minute with 5:1 ratio of compression to
ventilation
• If 1 man rescue: 80-100 compressions per
minute with ratio of 15:2 compression –
ventilation
• Most common complication of CPR :
FRACTURED RIBS
• Most common punctured organ: LIVER
When do we stop CPR?
• When the client is revived
• When the client has been pronounced death
• When the rescuer is exhausted
Nursing Management:
A. Promoting Oxygenation and Tissue
Perfusion
a. Instruct client to avoid
overfatigue ; stop activity
immediately when symptoms
manifest
b. O2 therapy by cannula on the
first 24 to 48 hours or longer if
pain persists
c. Position the client in semi-
fowlers position
B. Promoting Adequate Cardiac Output
a. Monitor the client for the
development of dysrrhythmias
b. Administer Pharmacotherapy
as prescribed
C. Promoting Comfort
a. Administer Morphine Sulfate
as prescribed
D. Providing Rest
a. Client is usually placed on bed
rest with commode previleges
for 24-48 hours
b. Administer diazepam (Valium)
E. Promoting Activity
a. Gradual increase in activity as
tolerated in encouraged
 b.
Stop any activity that causes
symptoms to manifest FACT:
F. Promoting Nutrition and Elimination
a. Provide small, frequent The heart has a specialized system for generating
feedings rhythmic electrical impulses and for conducting these
b. Provide low-cholesterol, low- impulses all throughout the heart
fat and sodium diet
c. Avoid stimulants such as Normally the heart pumping starts from atrial
caffeinated beverages contraction followed by ventricular contraction
d. Avoid straining during
defecation. Valsalva maneuver These coordinated contractions of the heart allows
changes blood pressure leading blood to be effectively pumped out all throughout
to development of body tissues and organs
dysrhythmias which may
trigger ischemia and cardiac The heart rhythm and conduction system is
arrest susceptible to damage especially during periods of
e. Administer stool softener as ischemia in the heart, which results to abnormal heart
ordered rhythms that causes the heart’s functions of supplying
G. Teaching and Counseling blood to various body organs to be impaired even
a. Discontinue Smoking leading to death.
b. Control hypertension with
continued medical supervision Main result of dysrythmia: REDUCTION OF
c. Maintain a low sodium low fat CARDIAC OUTPUT
diet
d. Progressive exercise as
tolerated CONDUCTION PATHWAY OF THE HEART:
e. Stress Management techniques
f. Resumption of Sexual
Activities
i. Assume a less tiring
position
ii. The non-MI partner
takes the active role
iii. Perform sexual
activity in a cool and
familiar environment
iv. Take nitroglycerine
before sexual activity
v. Refrain sexual
activity during a
fatiguing day
vi. If dyspnea, light
headedness, fatigue Electrical impulses are generated by the physiologic
occurs stop sexual pacemaker of the heart, the SA node. It signals atrial
activity immediately contraction as the impulse travels down the AV node
via the anterior, middle and posterior internodal
pathways. In the AV node, a delay of the impulses is
done to allow complete emptying of the atrial blood
content to the ventricles. The AV node then transmits
CARDIAC DYSRHYTHMIAS the impulses to the Bundle of His, which delivers the
impulse to the apex of the heart, signaling the start of
ventricular contraction Ventricular contraction is then
completed as the impulse spreads through the right
Cardiac Dysrhythmias are disturbances in the and left Bundle Branches.
regular heart rate or rhythm due to changes in the
Electrical conduction or automaticity in the heart.
ETIOLOGY AND RISK FACTORS:
(For pathophysiology of Cardiac dysrhythmias
Dysrhythmias can occur from disturbances in 3 major please refer to Appendix B)
mechanisms:
1. Automaticity Clinical Manifestations:
2. Conduction
3. Reentry of Impulses • Palpitations, which can be skipping,
pounding or fluttering in nature
• Fatigue
AUTOMATICITY • Chest pressure or pain
• Shortness of breath
Used to describe problems in the heart rate • Fainting, also known as syncope or near
produced by various pacemaker cells in the syncope
myocardium
• Light headedness or dizziness
The SA node is the normal pace maker of
Diagnostics:
the heart because it possesses the highest level of
automaticity (60-100 bpm). It is regulated by the
Electrocardiogram
Autonomic Nervous System through the Vagus
Nerves.
WAVES, COMPLEXES AND INTERVALS
There are times when the SA node fails to
The ECG is composed of waveforms
initiate the impulse. The body then makes use of its
alternative ESCAPE PACEMAKERS. The latent
pacemakers of the AV node assume the function of
being the body’s pacemaker whenever the SA node
fails to do so. But the intrinsic rate of the AV node is
lesser compared to that of the SA node (40-60 bpm).
If ever the AV node also fails to act as the escape
pacemaker, the pacemakers n the ventricles do the
job in a much lesser rate (<40 bpm).

Under a variety of circumstances, other cells

of the heart which also has the capacity to initiate
impulses create ECTOPIC BEATS. They are called
Ectopic Pacemakers.
P WAVE
CONDUCTION • sinus node spreading through the atria
• Atrial depolarization
Conduction of the heart is altered and does not follow QRS COMPLEX
the normal route correctly. This may be due to • Ventricular muscle depolarization
cardiac ischemia, scarring of the conduction • Normally less than 0.12 sec
pathways, and conduction of the nodes by scar T-WAVE
tissues, Myocardial infarction or effects of Beta • Ventricular muscle repolarization
Blocker Medications. • Resting rate of ventricles
• Amplitude less than 5mm
The conduction of blocked routes take longer time to U-WAVE
reach their destination, thus the wave becomes larger • Repolarization of the purkinje fibers
than usual. • Seen in patients with hyppokalemia,
hypertension, heart disease
RE-ENTRY OF IMPULSES • Follows the T-wave but smaller than the T-
wave
Reactivation of the cardiac muscles for the second
time by the same impulse initiated by the pacemaker. HOW TO READ AN ECG READING
Impulses are not extinguished but persists because of
a combination of slow conduction and blocks.
ECG INTERPRETATION

Step 1 : Calculate the heart rate Step 3: Examine each wave and segment for any
How? abnormality
a. Count the number of R waves in a 6- P-WAVE
inch strip of the ECG. Multiply the • Is one present for each QRS
number of R waves with 10. This will complex?
give you the estimated heart rate of the • Are they replaced by other wave
client forms?
• Are they identical or do they
change form?

Interpretation : 9 R waves x 10 = 90 bpm

Interpretation: Normal P waves with 1 P
wave every QRS complex

b. Count the number of large squares P-R INTERVAL

between R waves. Follow the following • Are they prolonged? They would
conversion: mean a heart block is present
1 large square = 300 bpm
2 large squares = 150 bpm
3 large squares = 100 bpm
4 large squares = 75 bpm
5 large squares = 60 bpm
6 large squares = 50 bpm
7 large squares = 43 bpm
Normal: 0.12 seconds- 0.20 seconds (3-5
8 large squares = 37 bpm
small boxes)
9 large squares = 33 bpm
Interpretation: 0.12 seconds (3 small boxes)
10 large squares = 30 bpm
Normal

Q-WAVES
• Look for pathological Q-waves
o Q waves greater than 3
mm in depth
o Q waves larger than 1/3
the R-wave
Interpretation: one small box less than 100 ~
90 bpm

Step 2: Determine the rhythm

Is the rhythm Regular? Irregular? Regularly Interpretation: Normal
Irregular? Irregularly Irregular
QRS WAVES
• Are they identical?
• DO they fall early? Indicative of
Premature Ventricular Contraction
• Are they wide and bizarre?
Occupying more than 3 small
Interpretation: Regular blocks in the ECG strip

Normal: 0.04-0.12 seconds (1 to 3 smal
boxes)
Interpretation: 0.08 boxes (2small boxes)
Normal
S-T SEGMENT
• Is the S-T segment elevated?
Myocardial Infarction
• Is it depressed? Ischemia
Interpretation: Normal
Normal ST Segment
ST Segment Elevation
ST Segment Depression
T-WAVE
• Is it inverted?
T-wave Inversion
Peaked T waves
C. Holter Monitoring
D. Treadmill Testing
DIFFERENT DYSRYTHMIAS:
SINUS DYSRYTHMIAS
Normal Sinus Rhythm
Also known as regular sinus rhythm. Most common
adult rhythm with rates 60-100 beats per minute. The
QRS is most often narrow with upright P waves in
Lead II
Sinus Bradycardia
With rates lesser than 60 beats per minute and may
be well tolerated by healthy adults. Adults may be in
routinely sinus bradycardia due to an optimal cardiac
stroke volume that requires less HR to yield
acceptable cardiac output
This can also be caused by:
• Increased vagal tone
• An effect of drugs such as the use of
digitalis, beta-blockers, or quinidine
• Sleep
• Seizure
Treatment:
• Atropine 0.5 to 1.0 mg/ IV push to block
vagal stimulaton
• Isoproterenol 1 mg/500 ml D5W to
stimulate sympathetic response
• Pacemaker
Sinus Tachycardia
A rhythm with elevated rate of impulse origination;
from the sinoatrial node, defines as a rate greater than
100 beats per minute in an average adult. Sinus
Tachycardia is a normal response to normal
physiologic conditions such as exercise and an
increased sympathetic tone as with increase
catecholamine release and stimulation.
Treatment:
• Digitalis administration
• Treat underlying cause
ATRIAL DYSRHYTHMIAS
Premature Atrial Contractions
A type of premaure heart beat, irregular heart beat or
benign arrhythmia which start in the upper two
chamber of the heart, also called the atria. These This may be due to conduction delay in the AV node.
aren’t as serous as premature ventricular contractions The impulse is transmitted normally but is delayed at
and usually do not require medical interventions. he level of the AV node. The management includes
Often people with premature atrial contractions suffer identifying and correcting electrolyte imbalances and
from palpitations. Usually caused by ectopic beats. withholding any offending medications. This
condition does not require admission unless there is
Treatment: an associated myocardial infarction.
• Generally does not require treatment
• Calcium Channel Blockers or Quinidine if Second Degree AV block
frequency inceases
Some but not all of the impulses form the SA node
Paroxysmal Atrial Tachycardia are transmitted by the AV node. The AV node
becomes selective on which impulses to be
A sudden onset of an atrial tachycardia with rates that transmitted.
vary between 140-250 beats per minute
Type I (Winkebach or Mobitz Type I)
Treatment:
• Valsalva Maneuver Occurs due to progressive slowing of the AV node.
• Digitalis This results to a lengthening of the PR interval
• Beta adrenergic Blockers followed by a dropping of the QRS complex- a P
wave not partnered with a QRS complex. The
• Calcium Channel Blockers
ventricular rhythm is then irregular. This may be
• Cardioversion caused by increased vagal tone, myocardial ischemia
• Morphine Sulfate, Diazepam or the effects pf drugs such as calcium channel
blockers and beta blockers.
Atrial Flutter
Type II or Mobitz Type II
A dysrhythmia in which an ectopic atrial focus
captures the heart rhythm and discharges impulses at Occurs below the AV node usually at he Bundle
a rate between 200-400 times per minute Branches or in the Bundle of His. Note that one or
more QRS complex is dropped with PR intervals
Treatment: remaining equal. This irregular rhythm requires
• Digitalis Preparation close monitoring since the dropped QRS causes
• Quinidine cardiac output to decrease and this heart rhythm can
• Calcium Channel Blockers proceed to complete heart block.
• Beta Adrenergic Blockers
• Cardioversion Third or Complete AV Block

Atrial Fibrillation
Is a type of arrythmia where the two atrias quiver
instead of contracting. It is caused by firing of
impulses from a multitude of foci.
Requires close monitoring for low cardiac output and
progression to asystole. Significant characteristics are
regular R-R interval with chaotic P-R intervals. No
impulse from the SA node is transmitted by the AV
node.

Treatment: Treatment of Choice for AV Blocks: Ventricular

• Digitalis Pacemaker
• Quinidine
• Beta adrenergic Blockers
VENTRICULAR DYSRHYTHMIAS

CONDUCTION DEFECTS/ HEART BLOCKS/ Premature Ventricular Contraction

AV BLOCKS
Also known as ventricular premature beat or
First Degree AV block extrasystole, is a form of irregular heartbeat in which
the ventricle contracts prematurely. This may be
perceived as a skipped beat or as palpitations. It is a
dysrythmis that is produced by an ectopic beat
originating in a ventricle and is being discharged at a
rate faster than that of the next occurring beat.
Life threatening if:
c. greter than 6 PVCs in a minute
d. Various configurations of PVCs are
present
i. Bigeminy (N-PVC-N-
PVC)
ii. Trigeminy (N-N-PVC-N-
N-PVC)
iii. Quadrigeminy (N-N-N-
PVC-N-N-N-PVC)
e. Occurs as two or more
consecutively
Treatment:
• Lidocaine / IV push, drip
o Initial bolus dose: 75-100 mg then
50-100 mg within 10-15 minutes as
needed
o Continuous IV drip in D5W 4:1
concentration
• Procainamide IV push, drip 300mg
• Bretylium / continuous infusion if lidocaine
and procainamide are ineffective
Ventricular Tachycardia (V-tach or VT)
Is a tachycardia, or fast heart rhythm that originates
in one of the ventricles of the heart. This is a
potentially life-threatening arrhythmia because it may
lead to a ventricular fibrillation and sudden death.
This is an emergency. Rate is usually 140-220 beats
per minute.
Treatment:
• Lidocaine, bolus dose followed by a
continuous IV drip from 1-4 mg /min
• Defibrillation if loss of consciousness occurs
• Cardioversion if conscious
Ventricular Fibrillation (V-fib or VF)
Is a condition in which there is uncoordinated
contraction of the cardiac muscle of the ventricles in
the heart, making them tremble rather than contract
properly. Ventricular fibrillation is a medical
emergency. If the arrhythmia continues for more than
a few seconds, blood circulation will cease, and death
may occur in a matter of minutes. Rate is greater than
300 beats per minute
Treatement:
• Immediate defibrillation, use 200-400
watt/sec (joules)
• Na Bicarbonate to relieve lactic acidosis
which causes unsuccessful defibrillation
• Epinephrine
Asystole
flatline
Medical Management:
CARDIOVERSION
Treatment of
choice for
arrythmias that
do not respond
to Vagal
maneuvers and
drug therapy.
Mechanism:
Cardioversion works by delivering an electrical
charge to the myocardium at the peak of the R wave.
This causes depolarization of the ventricles of the
heart, preventing the re-entry of ectopic focal beats
allowing the SA node to regain control.
Do not deliver on the T-wave since it causes
disruption of repolarization
Nursing Responsibilities:
1. Obtain an informed consent
2. Withhold all foods and fluids 6-12 hours prior to
the procedure
3. Obtain a 12-lead ECG to serve as your base line
data
4. Connect patient to pulse oximeter and automatic
BP cuff if available
5. Administer oxygen 5-10 minutes prior to
cardioversion to promote myocardial oxygenation.
but remove oxygen delivery device just before
cardioversion to prevent combustion.
6. Have a handheld resuscitation bag, an airway,
epinephrine, lidocaine and atropine at bedside
7. Hook an IV site in case drug administration is
necessary
8. Administer a sedative as ordered. The patient
should be heavily sedated but must be able to breathe
9. If the patient is attached to a telemetry machine,
remove the unit before cardioversion since the
electric shock may damage the unit
10. Avoid direct application of electric shock on pace
makers if present.
11. Place the client in a flat and firm surface and
apply interface material to the paddles
12. Give command for personnel to STAND CLEAR
of the client and the bed
13. Apply chest paddles as follows: one at the right of
the sternum, third ICS; and the other on the left mid
axillary fifth ICS
14. Push the discharge button on paddles
simultaneously
DEFIBRILLATION
Defibrillation is the
standard treatment for
ventricular fibrillation.
It involves using
electrode paddles to
direct an electric current
through the patient’s
heart.
Because ventricular
fibrillation occurs quickly and can cause death, the
effects of fibrillation is highly dependent on quick
and early identification of the arrhythmia.
Mechanism:
The current delivered by defibrillation causes the
myocardium to depolarize, which in turn encourages
the sinoatrial node to resume control over the heart’s
electrical activity.
Nursing Responsibilities:
1. Assess the patient if he lacks pulse. Call for help
and immediately perform CPR until the defibrillator
and other emergency equipments arrive
2. Expose the client’s chest and apply conductive
pads at the paddle placement positions or apply gels
to the paddles. Place one paddle at the right of the
upper sternum, just below the clavicle and the other
over the fifth or sixth intercostal space at the left
anterior axillary line.
3. Turn on the defibrillator and set the energy level at
200 joules for an adult person
4. Place the paddles over the conductive pads (if
used), and press firmly applying 11 kg of pressure
5. Instruct all personnel to stand clear of the patient
and the bed
6. Discharge the current by pressing both paddle
charge buttons simultaneously
7. Reassess the client’s cardiac rhythm and have
someone else assess the client’s pulse
8. If necessary prepare to defibrillate a second time,
using 300 joules of energy.
9. If defibrillaton is once again necessary, defibrillate
for the 3rd time using 360 joules of energy
10. In documenting defibrillation, do not forget to
chart: that the procedure was performed, patient’s
ECG rhythm before and after the procedure, number
of times defibrillation was performed, voltage used
during each attempt, whether a pulse returned,
dosage, route and time of drug administration,
whether CPR was done, means of airway
maintenance and patient’s outcome.
PACEMAKERS
TRANSCUTANEOUS PACEMAKERS
A temporary form of pacemakers
The device works by sending electrical impulses
from the pulse generator to the patient’s heart by way
of two electrodes, which are placed on the back and
the front of the patient’s chest.
Used only until the doctor can institute transvenous
pacing
TRANSVENOUS PACEMAKERS
More reliable compared to that of your
transcutaneous pacemakers
Involves threading an electrode catheter into the
cephalic or jugular vein into the patient’s right atrium
or right ventricle
The electrode then attaches to an external pulse
generator
The pulse generator can directly initiate impulse
towards the myocardium
PERMANENT PACEMAKER INSERTION
A self contained device designed to last for 3-20
years. The surgeon implants the pacemaker beneath
the client’s skin
Today, Permanent Pacemakers function in a demand
mode, allowing the patients heart to function on its
own while preventing it from falling to a preset rate
Nursing Responsibilities:
1. Clean incision site with soap and water
 2. Notify if swelling, redness and drainage b. Fatigability – from low in
occurs cardiac output, nocturnia,
3. Perform a 1 minute pulse check daily and insomnia, dyspnea, syncope,
notify doctor if heart rate changes occurs dizziness
4. Carry identification card at all times c. Insomnia and Restlessness
5. Avoid heavy lifting after 4 weeks d. Tachycardia
6. Avoid direct comfort to high powered CB
radios and other large running motors B. Right Sided Heart Failure
7. Avoid MRI a. Signs and Symptoms of
8. Repeat fast or slow heart beats, dizziness, elevated pressures and
shortness of breath or swollen ankles or feet congestion in systemic veins
9. Keep regular doctor appointments and capillaries
i. Edema of ankles,
weight gain (pitting
edema)
HEART FAILURE ii. Liver congestion—
may pproduce upper
abdominal pain
iii. Distended neck veins
Also called congestive heart failure (CHF) is a iv. Nocturia due to
clinical syndrome that results from the heart’s diuresis
inability to pump the amount of oxygenated blood v. Weakness
necessary to meet the metabolic requirements of the
body. C. Cardiovascular Findings in both sides
a. Cardiomegaly
Classified into 2: b. Ventricular gallop
f. Left Sided Heart Failure – Forward c. Rapid heart rate
Failure d. Development of Pulsus
g. Right Sided Heart Failure – alternans
Backward Failure
Diagnostic:
Clinical Manifestations: a. ECG may show ventricular hypertrophy
A. Left Sided Heart Failure and strain
a. Congestion occurs mainly in b. Echocardiography may show
the lungs from backing up of ventricular hypertrophy, dilation of
bloodinto the pulmonary veins cha,bers and abnormal wall motion
and capillaries c. Chest X-ray may show cardiomegaly,
i. Shortness of breath, pleural effusin and vascular congestion
dyspnea on exertion, d. ABG may show hypoxemia
paroxysmal nocturnal e. Liver function studies may be altered
dyspnea ( due to due to congestion
reabsorption of
dependent edema that Medical Management:
has developed
through the day), GOALS:
orthopnea, pulmonary a. Eliminating excess body fluids
edema b. Increasing the force of contraction and
ii. Cough—may be dry, efficacy of the heart
unproductive, often c. Reducing the workload of the heart
occurs at night. Rales,
Crackles, Moist 1. Diuretics
cough, Blood tinged c. Eliminates excess body water and
frothy sputum, decrease ventricular pressures
Wheezing d. Accompanied by a low sodium diet to
improve effectivity of therapy
2. Positive Inotropic Agents
 • Impproves the ability of the heart to
contract more effectively by
improving the contractile force of
the muscle
• Examples : Digoxin, Dopamine
(Intropin), Dobutamine (Dobutrex)
and Milrinone (Primacore)
Amrnone (Inocore)
3. Vasodilator Therapy
• Decreases the workload of the heart
by dilating the peripheral vessels.
This decreases ventricular preload
and volumes
• Examples: Nitrates
(Nitroglycerine), Hydralazine
(Apresoline), Prazosin (Minipress),
Sodium Nitroprusside (Nipride),
Morphine Sulfate (Dura Morph)
4. Angiotensin-Converting Enzyme
Inhibitors (ACE Inhibitors)
• Inhibits the vasoconstricting
capacity of the ACE
• Decreases left ventricular afterload
with a subsequent decrease in heart
rate thereby reducing cardiac
workload
• Examples: Captopril (Capoten),
Enalapril (Vasotec)
7. Beta adrenergic Blocking Agents (Beta
Blockers)
• Blocks the sympathetic effects of
epinephrine and norepinephrine on
the heart
• Examples: Selective: Metoprolol
(Lopressor) non-selectove:
Carvedilol
8. Diet
• Low sodium with fluid restrictions
9. Surgery
• Heart Transplant
• Phlebotomy
o Dry phlebotomy or
rotating tourniquets
intends to allow pooling of
blood in the lower
extremities, thereby
reducing preload
o Three extremities are
occluded at a time
o Rotate tourniquets
clockwise every
15minutes; each extremity
is occluded for a
maximum of 45 minutes
o If BP cuff is used as
tourniquet, inflate BP up
to 10-40 mmHg more than
the diastolic pressure
o Perform neurovascular
check distal to the
tourniquet : Pallor,
Paresthesia,
Poikilothermia, Pain
o Avoid too tight tourniquet
application as ischemia
may occur
Nursing Management:
A. Maintaining Adequate Cardiac Output and
Improving Circulation
a. Place patient at physical and
emotional rest in order to reduce
work of the heart
b. Place client in semi recumbent
position in an air conditioned
environment
c. Provide bedside commode
d. Provide psychological rest by
promoting physical comfort, avoid
anxiety
e. Monitor for progression of left
ventricular failure
i. Observe lowering systolic
blood pressure, and
narrowing pulse pressure
ii. Note for alternations of
weak and strong pulses
iii. Auscultate and Monitor
for S3 gallop and S4
sounds : common in CHF
iv. Monitor for premature
ventricular beats
f. Monitor for signs of poor systemic
circulation
g. Administer pharmacotherapy as
ordered
h. Supports lower arms with pillows
i. Auscultate lung fields every four
hours for presence of crackles and
wheezes
j. Change position of client
frequently every 2 hours
k. Encourage deep breathing exercises
l. Offer small frequent feedings to
prevent overdistention of stomach
reducing space for lung expansion
 m. Administer oxygen as directed
B. Restoring Fluid Balance
a. Administer prescribed diuretics and
give it AM
b. Input and Output recording must be
initiated
c. Weigh patient daily
d. Give oral potassium as prescribed
if taking Loop diuretics
e. Observe for signs of electrolyte
depletion : lassitude, apathy, mental
confusion, anorexia, decreasing
urinary output
f. Limit Oral Fluid Intake as well as
IV infusions
g. Monitor for pitting edema on lower
extremities and sacral area. Use egg
crate mattress and sheep skin to
prevent pressure soars
h. Be alert for complains of right
upper quadrant pain. May indicate
liver congestion
i. Avoid salt in diet
C. Improving Activity Intolerance
a. Improve patient’s activity gradually
according to limitations
b. Frequently monitor patient’s heart
rate during activity and be alert for
complains of chest pain or skeletal
pain
c. Relieve for night time anxiety and
provide rest and sleep
Functional Capacity Classification of Patients
with Heart Diseases:
Class I: Patients with cardiac disease but
with no limitations of physical activity.
Class II: Patents with cardiac disease but
with slight limitations of physical activity.
Comfortable at rest. Ordinary physical
activity results in fatigue, palpitations,
dyspnea and or angina
Class III : Patients with cardiac disease
resulting in marked limitation of physical
activity. They are comfortable at rest. Less
than ordinary physical activity causes
symptoms.
Class IV: Patients with cardiac disease
resulting in inability to carry on any physical
activity without discomfort. Symptoms
occur even at rest.
Therapeutic Classifications of Patients with Heart
Diseases:
Class A: Patients with cardiac disease
whose ordinary physical activity need not be
restricted
Class B: Patients with cardiac disease
whose ordinary physical activity need not be
restricted but should be advised against
severe or competitive physical efforts
Class C: Patients with cardiac disease
whose ordinary physical activity must be
moderately restricted and whose more
strenuous efforts should be discontinued
Class D: Patients with cardiac disease
whose ordinary physical activity should be
markedly restricted
Class E: Patients with cardiac disease who
should be at complete bed rest, confined to
bed or chair.
VALVULAR DEFECTS
The function of normal heart valves is to maintain the
forward flow of blood from the atria to the ventricles
and from the ventricles to the great vessels.
Valvular damage may interfere with valvular
function by stenosis or by impaired closure that
allows backward leakage of blood (valvular
insufficiency, regurgitation and incompetence).
Mitral Stenosis
Progressive thickening and contracture of
valve cusps with narrowing of the orifice and
progressive obstruction to blood flow. The left atrium
has difficulty in emptying itself into the left ventricle,
therefore it dilates and hypertrophies. As a result of
the abnormally high pulmonary arterial pressure that
must be maintained, the right ventricle is subjected to
a pressure overload and may eventually fail.
Mitral Insufficiency
 Incomplete closure of the mitral valve Medical Management:
during systole, allowing blood to flow back into the a. Antibiotic therapy for prophylaxis for
left atrium. Left Ventricle and Right Ventricle may endocarditis before invasive procedures
hypertrophy as a result of backflow of blood. b. Treatment of heart failure – diuretics,
vasodilators, cardiac glycosides as
Aortic Stenosis indicated
c. Surgical Intervention:
Narrowing of the orifice between the left a. Mitral Stenosis
ventricle and the aorta. The obstruction to the aortic i. Closed Mitral
outflow places a pressure load on the left ventricle Valvotomy
that results in hypertrophy and failure. ii. Open Mitral
Valvotomy
Aortic Insufficiency iii. Mitral Valve
Replacement
Valve flaps fail to completely seal the aortic iv. Baloon Valvuloplasty
orifice during diastole and thus permit backflow of b. Mitral Insufficiency
blood from the aorta into the left ventricle. The left i. Mitral Valve
ventricle increases the force of contraction to Replacement
maintain adequate cardiac output often resulting in ii. Annuloplasty
hypertrophy. c. Aortic Stenosis and
Insufficiency
Tricuspid Stenosis i. Aortic Valve
Replacement
Restriction of the tricuspid valve orifice due ii. Balloon
to commissural fusion or fibrosis Valvuloplasty
d. Tricuspid Stenosis or
Insufficiency
Tricuspid Insufficiency i. Valvuloplasty
ii. Tricuspid Valve
Allows regurgitation of blood from the right Replacement
ventricle into the right atrium during ventricular
systole Nursing Management:

Clinical Manifestations: A. Maintaining adequate Cardiac Output

a. Fatigue
b. Dyspnea, cough, orthopnea,
nocturnal dyspnea and murmurs
c. Dysrhythmia, palpitations
d. Hemoptysis
e. Low blood pressure, dizziness,
syncope, angina, symptoms of CHF
f. Neck vein distention and visible
and palpable arterial pulsations
over the precordium
Diagnostic Evaluation:
a. Echocardiography may show
abnormalities of valve structure and
chamber size and thickness
b. Chest X-ray shoes signs of
cardiomegaly and pulmonary vascular
congestion
c. Cardiac catheterization and
angiocardiography
a. Assess frequently for presence of
murmurs
b. Assess for signs of let and/or right
ventricular failure
c. Monitor and treat dysrhythmias as
ordered
d. Prepare patient for surgical
operation
B. Improving Tolerance
a. Maintain bedrest until symptoms of
CHF are present
b. Allow patient to rest between
interventions
c. Begin activities gradually as
tolerated
d. Assist or perform hygiene needs
and other needs of the client
C. Patient Education
a. Review activity restriction/schedule
with patient and family
b. Instruct patient and SO to report
signs of worsening heart failure
c. Review Sodium and Fluid
restrictions

Prepared by:
Mr. Jerald S. Ugdoracion, RN, MN-MSN
(please do not reproduce without permission)