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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 c.Provide diversional activities that
fever (e.g. Prednisone, Aspirin) prevents exertion
3. Digoxin, Diuretics (Furosemide and D. Patient Education
Spironolactone) and Supplemental O2 is a. Counsel the patient on hygienic
given among clients who developed practices
congestive heart failure after RHD. b. Counsel on the importance of
i. Check Potassium levels of adequate nutrition and rest periods
patient prior to initiating c. If sore throat occurs, tell patient to
digoxin therapy to prevent immediately seek medical
possibility of toxicity consultation
ii. Loading dose : 1.25-1.5
mg/d Maintenance dose:
0.25-0.5 mg/d INFECTIVE ENDOCARDITIS
Therapeauic Level: 1.5-2
ng/ml An infection on the valves and the endothelial surface
4. Rest – to maintain optimum cardiac function of the heart brought about by bacterial invasion that
5. Prevention of Recurrent episodes by Long may progress to deformities of the cardiac valves and
term use of penicillin (Penicillin G 0.6 to 1.2 cardiac insufficiency.
million units injections every 4 weeks for 5
years or until age 21 for patients with RHD Common Affecting Microorganisms:
without carditis but for 10 years or until age Streptococci, Pneumococci and Staphylococci, Fungi
40 for patients with RHD with carditis. and Rickettsiae
6. Surgical Management is only indicated
when severe valvular damage has already Other Risk Factors:
occurred to the heart that cardiac functioning a. Disorders on the valves of the
has already been impaired. heart
b. Age : more common among
Nursing Interventions: older people
c. Intravenous drug use
A. Reducing Fever d. Hospitalization : occurs
a. Administer penicillin therapy or commonly among patients
erythromycin therapy when allergic with debilitating disorders that
to penicillin requires indwelling catheters
b. Give salicylates as prescribed or prolonged IV access
c. Tae and record temperature every 3 e. Immunosuppression : Fungal
hours and evaluate comfort level of Endocarditis
patient for evaluation of drug
effectivity Complications: Valvular defects, heart failure,
B. Maintaining Adequate Cardiac Output embolism and poor perfusion to various
a. Assess for complains of chest pain, organs.
palpitations or precordial tightness,
tachycardia as this may indicate Clinical Manifestations:
development of carditis a. General manifestations of malaise,
b. Auscultate for murmurs or anorexia, weight loss and intermittent fever.
pericardial friction rub b. Roth’s Spots : hemorrhages with pale
c. Monitor the development of centers in fundi of eyes
chronic rheumatic endocarditis c. Osler’s Nodes : nodules that are small and
whichmay include valvular painful in pads of fingers or toes
disorders leading to CHF. d. Cardiac Manifestations: heart
C. Maintaining Activity enlargement, heart failure, heart murmurs
a. Maintain bedrest if fever persists or e. Varied manifestations according to areas
if signs of carditis are present of embolism (e.g. Myocardial
b. Provide active-assistive ROM Ischemia on heart, stroke on brain,
programs hematuria and renal failure on kidney)
Diagnostics:
a. Serial Blood Culture and
Sensitivity Clinical Manifestations:
a. Pain felt beneath the clavicle and in the
Medical Management: neck and left scapular region,
a. Adequate dosages of Antimicrobial aggravated by breathing, turning in bed
Agents depending on Causative Agent and twisting of body and is relieved by
(continuous IV infusion for 2-6 weeks) leaning forward or sitting up (Friction
b. Seriously damaged valves may rub)
require surgical intervention: Surgical b. Dyspnea
Valve Replacement c. Fever, High WBC count

Nursing Management: Cardiac Tamponade Clinical Manifestations:


a. Provide psychosocial support a. Falling BP, rising venous pressure
b. Provide post surgical care to clients if (distended neck veins), and distant
patient received surgical intervention (muffled) heart sounds with pulsus
c. Monitor patient’s temperature : Fever may paradoxus
be present for weeks b. Anxiousness, confusion and restlessness
d. Monitor for signs of Systemic Embolization c. Dyspnea, Tachypnea and Precordial
or poor organ perfusion Pain
e. Instruct patient and family about activity d. Elevated CVP
restrictions and signs and symptoms of
infection Medical Management:
f. Reinforce that antibiotic prophylaxis is a. Bed Rest is instituted when patient’s cardiac
recommended for patient who had previous output is severely impaired
Endocarditis and who are to be subjected b. Pharmacologic Therapy:
with invasive procedures a. Narcotic analgesics for Pain relief
g. Refer to home care nurse to supervise and during the acute phase
monitor intravenous antibiotics b. Analgesic and NSAIDS to hasten
reabsorption of fluid in the
pericardial sac ; Colchicine may be
PERICARDITIS an alternative medication
c. Corticosteroids
Inflammation of the pericardium , the membranous d. Penicillin : DOC if pericarditis is
sac enveloping the heart. Usually caused by viral due to rheumatic fever
infection but may be caused by bacteria and fungi at e. Isoniazid, Rifampicin,
times. Pyrazinamide, Ethambutol and
Streptomycin if pericarditis is
Can be classified by what accumulates in the caused by tuberculosis
pericardium: f. Amphotericin B if caused by fungal
a. Serum : Serous infection
b. Pus : Purulent
c. Calcium deposits : Calcific c. Surgical Management
d. Clotting Proteins : Fibrinous a. Pericardiocentesis : removal of
e. Blood : Sanguinous pericardial fluid
b. Pericardiectomy : removal of the
Complications: Pericardial Effusion, Cardiac tough encasing pericardium
Tamponade
Nursing Management:
a. Assess pain and possible presence of
precordial pain.
Picture Illustrating b. Monitor temperature frequently
Cardiac Tamponade c. Assess for presence of pericardial
friction rub. Differentiate Pericardial
Friction rub from Pleural Friction Rub
(audible upon auscultation and a. Monitor for digitalis toxicity for clients
synchronous with heartbeat and is who are receiving digitalis therapy :
continuous) Nausea, Anorexia, Vomiting, Diarrhea,
d. Advise bed rest or chair rest in sitting Bradycarda and Blurring of Vision
upright or leaning forward position b. Instruct patient to increase physical
e. Instruct patient to resume ADLs activity when tolerated and to report
gradually as tolerated when pain and any symptom that occur with increased
friction rub abate and to resume bedrest activity
when pain and friction rub recur c. Avoid competitive sports and alcohol
f. Monitor for triad manifestation of
Cardiac Tamponade : (1) Falling arterial
pressure (2) Rising venous pressure (3)
Distant heart Sounds. Report DEFICIENCY IN BLOOD SUPPLY TO THE
immediately if present to prevent HEART
cardiac tamponade and prepare for
pericardiocentesis
CORONARY ARTERY DISEASE (CAD) /
CORONARY ATHEROSCLEROTIC HEART
MYOCARDITIS DISEASE (CAHD)

An inflammatory process that involves the A condition characterized by abnormal accumulation


myocardium which results from an infectious process of lipid or fatty substances and fibrous tissues in the
(e.g. viral, bacterial, mycotic, parasitic, or protozoal) myocardial vessel wall reducing the blood flow to the
that may threaten life due to progressive myocardial myocardium. This is a progressive disease but can be
degeneration. curtailed and in some case reversed.

Clinical Manifestations: If not prevented then this can lead to Myocardial


a. Fatigue, Dyspnea, Palpitations and Infarction and Heart Failure
occasional discomfort in the chest
orupper abdomen Modifiable Risk factors:
b. Pericardial Friction rub if accompanied a. Cigarette Smoking
with pericarditis b. Elevated Blood Pressure
c. Fever c. High Blood Cholesterol
d. Pulsus alternans may be present (Hyperlipidemia)
d. Obesity
Complication: Heart Failure e. Diabetes Mellitus
f. Physical Inactivity
Assessment and Diagnostics: g. Use of Oral Contraceptives
a. Cardiac enlargement as revealed by h. Behavior patterns
cardiac roentgenography
b. Faint heart sounds upon auscultation Non-Modifiable Factors:
c. Gallops and murmurs may be present a. Positive Familial History : common among
d. Confirmatory diagnostic procedure : people with 1st degree relatives who suffered
ENDOMYOCARDIAL BIOPSY from cardiac disorders before age 50
b. Age : common among men more than 45
Medical Management: years old and women more than 55 years old
a. Bed rest to decrease cardiac workload c. Gender : occurs 3 times more in men than in
b. Continuous cardiac monitoring to detect women
possible dysrythmias d. Race: higher incidence among African
c. Digitalis use: to decrease the heart rate Americans
while improving contractility of the
heart Clinical Manifestations:
a. Chest Pain (Angina Pectoris)
Nursing Management:
b. Atypical symptoms of myocardial ischemia Special Nursing
(shortness of breath, nausea and unusual Considerations:
fatigue) a. Avoid giving Non-
c. Myocardial Infarction Selective Beta Blockers
(Propanolol) to clients
Medical Management: with impaired breathing
a. The goal of medical management is to pattern or with labored
decrease cardiac oxygen demand and breathing. May cause
increase O2 supply further respiratory
b. Pharmacologic Therapy is instituted depression.
especially if angina pectoris accompany b. Adjust dosages of
CAD: Insulin to diabetics.
• Fast Acting Nitrates (e.g. Propanolol can cause
Nitroglycerine) hypoglycemia
Action: Causes peripheral
vasodilation resulting to a • Anti-coagulants and Anti-platelet
decreased peripheral vascular Aggregation agents
resistance decreasing blood o Heparin and Warfarin
pressure and cardiac workload o Ticlopidine, Aspirin,
Special Nursing Considerations: Dipyridamole
a. Perform interventions that would Action: Prevents the formation
prevent complications of of clots by preventing the
Orthostatic Hypotension blood clotting cascade
b. Remember that fast acting nitrates Special Nursing
is the drug of choice for angina Responsibilities:
pectoris; take a maximum of three a. Assess for signs and
doses given in 5 minute interval. If symptoms of bleeding
not effective rush client to hospital b. Avoid straining on
c. Store nitroglycerine in cool, dark defecation
places and change every 6 months c. Monitor PT levels
d. Sublingual nitroglycerine is the (Coumadin therapy) and
fastest but may cause burning and PTT levels (Heparin
tingling sensation under the tongue therapy)
e. If using transdermal patches, d. Keep antidotes ready :
replace daily, wipe off before Protamine Sulfate for
replacement and rotate sites. Heparin and Vitamin K
Remove prior to defibrillation to for Coumadin therapy
avoid burns. e. Minimize vegetables in
f. Observe for common signs of drug the diet to decrease
effectivity – faintness, flushed extraneous sources of
appearance, dizziness, headache : Vitamin K
Do not discontinue the drug
• Calcium-Channel Blockers
• Beta Adrenergic Blockers o Verapamil
i. Propanolol (Inderal) o Nifidipine
ii. Metoprolol (Lopressor) o Diltiazem
iii. Nadolol (Cogard) Action: Blocks the influx of
iv. Atenolol (Tenormin) calcium in to the myocardium
v. Pindolol (Visken) decreasing the action potential
Action: Blocks the beta of the heart muscles
adrenergic sites of the heart Special Nursing
preventing epinephrine from Considerations:
performing its sympathetic a. Assess heart rate and BP
effects on the heart b. Monitor hepatic and renal
function
c. Administer 1 hr before or c. Coronary Artery Bypass Graft
2 hrs after meals. Food (CABG)
delays the absorption of i. Recommended if more
the medication than one branch of coronary artery is
narrowed by atheromatous plaques
c. Surgical Management: ii. Main Purpose :
a. Percutaneous Transluminal Myocardial revascularization
Coronary Angioplasty (PTCA) iii. Internal Mammary Artery
i. Mechanical dilation of the and Saphenous Vein : Most
coronary vessel wall by compressing commonly used grafts
the atheromatous plaque
ii. Recommended to clients Special Nursing Considerations:
with single vessel coronary artery • Prior to the operation, an IV line is
disease inserted to the client
iii. A specially designed • Client is placed on General
balloon tipped catheter is inserted Anesthesia
under fluoroscopic guidance and • Postoperatively, take the client to
advanced to the site of coronary the ICU for close cardiac
obstruction monitoring
• Monitor pacing wires and breathing
Special Nursing Considerations: and drainage tubes
• Prior to the operation, an IV line is • Monitors and tubes removed over
inserted to the client the next few days
• Client is placed on NPO 8 hours
prior to surgery and preoperative Please refer to this internet website for
sedative and medications are given additional information:
http://www.youtube.com/watch?
• Inform client that surgery may take v=MDKa1Do1lSU&feature=related
30 minutes to 1 hour
• Inform client that a feeling of
pressure may be felt upon insertion Nursing Management:
of the catheter and a flushing a. prevention of the development of CAD is
feeling may be felt when the focus
fluoroscopic dye is inserted a. Daily management of Hypertension
• Postoperatively, take the client to : Instruct to take medication at
the ICU for close cardiac regular basis and never to stop
monitoring unless told by prescriber
• Check for bleeding on femoral site b. Smoking cessation
and apply pressure bandage c. Avoid passive smoking
d. Plan a regular exercise under
medical supervision
Please refer to this internet website for e. Follow a healthy heart diet : Low
additional information: Sodium and Low Fat Diet
http://www.youtube.com/watch? f. Reduce stress
v=N7nghr9TpSU&feature=fvw
g. Allow adequate time for rest and
relaxation
b. Intravascular Stenting
i. Biologic stent is produced
through coagulation of collagen,
ANGINA PECTORIS
elastin and other tissues in the vessel
wall by laser, photocoagulation or
A transient chest pain caused by insufficient blood
radio frequency- induced heat
flow to the myocardium resulting in to myocardial
ii. Prosthetic intravascular
ischemia. It results when myocardial oxygen demand
cylindric stents maintain good
exceeds myocardial oxygen supply.
luminal geometry after balloon
deflation and withdrawal
Clinical manifestations:
a. transient, paroxysmal substernal a. Pharmacologic Therapy (similar to that
precordial pain of CAD, pls refer to Pharmacologic
b. heaviness or tightness of the chest that therapy for CAD)
radiates down to one or both arms, left b. Surgical Management (similar to that of
shoulder, jaw or neck and back CAD, pls refer to Surgical
c. Pain relieved by NITROGLYCERINE management for CAD)
d. Pallor, diaphoresis, dyspnea, faintness,
palpitations, dizziness Nursing Management:
a. Improve diet of the client. Change to
Types of Angina Pectoris: low sodium, low fat and high fiber diet
a. Stable Angina b. Improve activity of client according to
o Chest pain lasts for less than 10-15 what is tolerable to the client
minutes and recurrence is less c. Promote comfort
frequent d. Promote and improve tissue perfusion
b. Unstable Angina (Preinfarction Angina, e. Instruct patient to stop activity
Cresendo Angina, Intermittent immediately when symptoms manifest
Coronary Syndrome) f. Advise client to reduce emotional
o Chest pain lasts more than 15 outbursts, worry and tension
minutes but less than 30minutes
and recurrence is more frequent
while intensity increases
c. Variant Angina (Prinzmetal’a Angina) MYOCARDIAL INFARCTION
o Chest pain may last longer than that
of unstable angina and may even The formation of localized necrotic areas within the
occur at rest myocardium. Follows suddenly from abrupt cessation
o Attacks tend to occur at the early of blood and oxygen flow to the heart muscle.
hours of the day
d. Nocturnal Angina Prolonged ischemia lasting for more than 35 minutes
o Occurs only during at night and is can cause irreversible cellular damage and necrosis of
highly associated with rapid eye the myocardium. Alterations in function depends on
movement (REM) sleep the size and location of an infarct
e. Angina Decubitus
o Paroxysmal chest pain that occurs (for psychopathophysiology of Myocardial Infarction please see
Appendix A)
when the client sits or stands up
f. Intractable Anina
Classifications of Infarct:
o Chronic incapacitating angina
a. Transmural Infarct
unresponsive to intervention
g. Postinfarction Angina • Damage extends from endocardium
o Occurs after MI, when residual to epicardium
b. Subendocardial Infarct
ischemia may cause episodes of
anigina. • Affects the endocardial muscles
only
Precipitating Events of Angina Pectoris: c. Intramural Infarct
a. Exertion : too much exertion or • Seen in patchy areas of the
exercise done in a sporadic myocardium and is usually
manner associated with longstanding
b. Emotions : Excitement (e.g. angina pectoris
sexual activity)
c. Eating a very heavy meal Three Areas that Develop in Myocardial
d. Environment : Exposure to Infarction
very cold temperature a. Zone of Infarction
• Records pathologic Q waves in the
Collaborative Management: ECG
• Irreversible damage, death to the especially in the presence of
heart muscle due to extensive and elevated LDH levels
complete oxygen deprivation i. Shock
b. Zone of Injury • Systolic blood pressure below
• Records elevated ST segment 80 mmHg, lethargy, cold,
• Area of the heart muscle diaphoresis, peripheral
surrounding the area of necrosis, cyanosis,
inflamed and injured, but still tachycardia/bradycardia, weak
viable of adequate oxygenation is pulse
restored
c. Zone of Ischemia Diagnostics:
• Records inversion of T-wave a. Electrocardiogram
• Surrounds the area of injury, • MI causes elevation of ST
ischemic and viable segment, Inversion of T wave
and enlargement of Q wave
Clinical Manifestations:
a. Pain b. Cardiac Enzyme Studies
• Crushing, severe, prolonged a. Aspartate Aminotransferase (AST)
unrelieved by rest or NL: 7-40 mu/mL
nitroglycerine; often radiating • Formerly known as SGOT,
to one or both arms, the neck elevated levels indicate tissue
and the back. necrosis
• Characterized by Levine’s sign • Range with Myocardial
Infarction:
b. Anxiety and Apprehension o Initial Elevation : 4- 6
• Feeling of doom and hrs
restlessness o Peaks : 24-36 hrs
c. Oliguria o Returns to normal : 4-
• Urine flow less than 30 cc/hr 7 days
d. Fever b. Creatine Phosphokinase (Ck-MB)
• Slight elevation of temperature • It is the most specific cardiac
occurs within 24 hours and enzyme and is an accurate
extends 3 to 7 days indicator of Myocardial
accompanied by leukocytosis damage
and elevated ESR • Normal range: Males : 50-325
e. Indigestion mu/ml Females: 50-250
• “Gas pains around the heart” mu/mL
nausea and vomiting • Range with Myocardial
f. Acute Pulmonary Edema Infarction
• Sense of suffocation, dyspnea, o Onset: 3-6 hrs
orthopnea, gurgling/bubbling o Peaks: 12-18 hrs
respiration o Returns to normal: 3-
g. ECG changes 4 days
• MI causes elevation of ST c. Lactic Dehydrogenase (LDH)
segment, Inversion of T wave • LDH1 is the most sensitive
and enlargement of Q wave indicator of myocardial
h. Elevated CK-MB, Elevated LDH damage
and Elevated AST • In MI : LDH 1 is elevated and
• These cardiac enzmes are its level exceeds LDH 2. LDH
produced abnormally high 1/LDH2 ratio becomes flipped
because of cellular damage and • Normal range: 100-225 mu/mL
death • Range in Myocardial
• Rise of CK-MB is the most Infarction:
definitive findings in MI, o Onset: 12 hours
o Peaks : 48 hours c. Anticoagulant Therapy
o Returns to Normal: i. Administered after
10-14 days thrombolytic therapy to
d. Troponin I and T maintain patency of
• Protein components coronary arteries
found on striated ii. Examples : Heparin and
muscles specific to the Coumadin
heart d. Other Antihypertensives
• Troponin T (84% i. Beta-Adrenergic Blockers
sensitivity o MI) ii. Calcium Channel Blockers
Troponin I (90 % iii. Angiotensin Receptor
sensitivity toMI) Blockers
• Range in Myocardial
infarction: B. Treatment
a. Goals:
• Onset: 3-6 hours
i. Prevention of further
• Peak: 20 hrs
tissue damage and
• Lasts longer than that of limitation of infarct size
Ck-MB ii. Maximize myocardial
Complications: tissue perfusion and
Complications include arrhythmia, cardiogenic reduce myocardial tissue
shock, heart failure, pulmonary edema, cerebral or demands
pulmonary emboli, myocardial rupture, pericarditis, b. Supplemental Oxygen by Nasal
postmyocardial infarction syndrome, and sudden Cannula
death. c. Cardiac Monitoring to monitor
development of dysrhythmias
Collaborative Management: d. PTCA may be done to reopen
occluded arteries
A. Pharmacologic Therapy e. Diet: Low sodium Low fat diet
a. Analgesics f. Activity: Bed Rest is usually
i. For pain relief. Important prescribed for 24-48 hours to
because pain can cause decrease oxygen demand.
shock. Progressive ambulation is
ii. DOC: Morphine Sulfate, implemented as soon as possible,
Lidocaine or unless complications occur.
Nitroglycerine
administered IV
b. Thrombolytic Therapy CARDIOPULMONARY RESUSCITATION
i. DOC: Streptokinase, (CPR)
Urokinase, and TPA
(Tissue Plasminogen Indicated during cardiopulmonary arrest
Activators) (breathlessness, pulselessness or clinical death) and is
ii. Administered between 3-6 instituted within 4-6minutes after the arrest to prevent
hours after the initial brain damage.
infarction has occurred
iii. Given in order to lyse Two Types of CPR:
blood clots that may have a. BLS – Basic Life Support
occluded one of the major
• involves the use of
arteries supplying blood
hands, mouth and the sincere
and oxygen to the heart
desire to give a person a
causing the infarction
second chance of life
iv. Nursing responsibilities
b. ACLS – Advanced Cardiac Life
include monitoring the
Support
client for bleeding and
• Involves BLS and the
assessment of neurologic
use of equipments,
status
emergency drugs and
fluids to monitor the Step 5: Initiate External Cardiac Compressions
client and stabilize his • Place the heel of one hand on the area of 2
condition fingerbreadths from the xiphoid process
(adult); midsternum of the infant
CPR involves the ABCD of life support: • Depress the sternum with heels of both
A – Airway hands (dominant hand over non-dominant
B – Breathing hand) 1 ½ - 2 inches for adults, heel of one
C – Circulation hand 1 ½ - 2 inches for children and 2
D – Definitive treatments fingers ½ - 1 inch for infant
• If 2 rescuers: 80-100 compressions per
TECHNIQUES OF BASIC LIFE SUPPORT minute with 5:1 ratio of compression to
ventilation
Step 1: Assess LEVEL OF CONSCIOUSNESS • If 1 man rescue: 80-100 compressions per
• Shake the victim’s minute with ratio of 15:2 compression –
shoulders and asl “Are you ok?” ventilation
• If no response, place the • Most common complication of CPR :
client in a Supine position on a firm surface FRACTURED RIBS
• Most common punctured organ: LIVER
Step 2: Open the AIRWAY
• The tongue is the most common cause of When do we stop CPR?
airway obstruction in an unconscious person • When the client is revived
• Use the HEAD TILT-CHIN LIFT • When the client has been pronounced death
MANEUVER and the JAW THRUST • When the rescuer is exhausted
methods for opening and maintaining airway
• Jaw thrust is recommended for clients with
suspended neck injury Nursing Management:
• Take 3 to 5 seconds to look , listen and feel A. Promoting Oxygenation and Tissue
for spontaneous breathing 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 B a. Monitor the client for the
development of dysrrhythmias
Picture A – Jaw Thrust Maneuver
Picture B – Head Tilt Chin Lift Maneuver
b. Administer Pharmacotherapy
as prescribed
C. Promoting Comfort
Step 3: Initiate ARTIFICIAL VENTILATION a. Administer Morphine Sulfate
as prescribed
• Give 2 initial breaths lasting for 1 ½ to 2 D. Providing Rest
seconds. Watch for rise and fall of the chest a. Client is usually placed on bed
upon introduction of air. If no rise and fall rest with commode previleges
occurs, consider airway obstruction for 24-48 hours
b. Administer diazepam (Valium)
Step 4: Assess CIRCULATION E. Promoting Activity
• Check the carotid pulse (adult) for 5-10 a. Gradual increase in activity as
seconds, brachial pulse for infant and child tolerated in encouraged
• If no pulse, cardiac compression is initiated
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
DIFFERENT DYSRYTHMIAS:

SINUS DYSRYTHMIAS

Normal: 0.04-0.12 seconds (1 to 3 smal Normal Sinus Rhythm


boxes)
Interpretation: 0.08 boxes (2small boxes) Also known as regular sinus rhythm. Most common
Normal adult rhythm with rates 60-100 beats per minute. The
QRS is most often narrow with upright P waves in
S-T SEGMENT Lead II
• Is the S-T segment elevated?
Myocardial Infarction Sinus Bradycardia
• Is it depressed? Ischemia
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
Interpretation: Normal
This can also be caused by:
Normal ST Segment • Increased vagal tone
• An effect of drugs such as the use of
digitalis, beta-blockers, or quinidine
• Sleep
ST Segment Elevation
• Seizure

Treatment:
ST Segment Depression • Atropine 0.5 to 1.0 mg/ IV push to block
vagal stimulaton
• Isoproterenol 1 mg/500 ml D5W to
T-WAVE stimulate sympathetic response
• Is it inverted? • Pacemaker

Sinus Tachycardia

A rhythm with elevated rate of impulse origination;


T-wave Inversion
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.
Peaked T waves Treatment:
• Digitalis administration
• Treat underlying cause

ATRIAL DYSRHYTHMIAS
C. Holter Monitoring
D. Treadmill Testing 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 Requires close monitoring for low cardiac output and
progression to asystole. Significant characteristics are
Is a type of arrythmia where the two atrias quiver regular R-R interval with chaotic P-R intervals. No
instead of contracting. It is caused by firing of impulse from the SA node is transmitted by the AV
impulses from a multitude of foci. 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 Treatement:
originating in a ventricle and is being discharged at a • Immediate defibrillation, use 200-400
rate faster than that of the next occurring beat. watt/sec (joules)
• Na Bicarbonate to relieve lactic acidosis
which causes unsuccessful defibrillation
Life threatening if: • Epinephrine
c. greter than 6 PVCs in a minute
d. Various configurations of PVCs are Asystole
present
i. Bigeminy (N-PVC-N- flatline
PVC)
ii. Trigeminy (N-N-PVC-N- Medical Management:
N-PVC)
iii. Quadrigeminy (N-N-N- CARDIOVERSION
PVC-N-N-N-PVC) Treatment of
e. Occurs as two or more choice for
consecutively arrythmias that
do not respond
Treatment: to Vagal
• Lidocaine / IV push, drip maneuvers and
o Initial bolus dose: 75-100 mg then drug therapy.
50-100 mg within 10-15 minutes as
needed Mechanism:
o Continuous IV drip in D5W 4:1
concentration Cardioversion works by delivering an electrical
• Procainamide IV push, drip 300mg charge to the myocardium at the peak of the R wave.
• Bretylium / continuous infusion if lidocaine This causes depolarization of the ventricles of the
and procainamide are ineffective heart, preventing the re-entry of ectopic focal beats
allowing the SA node to regain control.
Ventricular Tachycardia (V-tach or VT) Do not deliver on the T-wave since it causes
disruption of repolarization
Is a tachycardia, or fast heart rhythm that originates
in one of the ventricles of the heart. This is a Nursing Responsibilities:
potentially life-threatening arrhythmia because it may
lead to a ventricular fibrillation and sudden death. 1. Obtain an informed consent
This is an emergency. Rate is usually 140-220 beats 2. Withhold all foods and fluids 6-12 hours prior to
per minute. the procedure
3. Obtain a 12-lead ECG to serve as your base line
Treatment: data
• Lidocaine, bolus dose followed by a 4. Connect patient to pulse oximeter and automatic
continuous IV drip from 1-4 mg /min BP cuff if available
• Defibrillation if loss of consciousness occurs 5. Administer oxygen 5-10 minutes prior to
• Cardioversion if conscious cardioversion to promote myocardial oxygenation.
but remove oxygen delivery device just before
Ventricular Fibrillation (V-fib or VF) cardioversion to prevent combustion.
6. Have a handheld resuscitation bag, an airway,
Is a condition in which there is uncoordinated epinephrine, lidocaine and atropine at bedside
contraction of the cardiac muscle of the ventricles in 7. Hook an IV site in case drug administration is
the heart, making them tremble rather than contract necessary
properly. Ventricular fibrillation is a medical 8. Administer a sedative as ordered. The patient
emergency. If the arrhythmia continues for more than should be heavily sedated but must be able to breathe
a few seconds, blood circulation will cease, and death 9. If the patient is attached to a telemetry machine,
may occur in a matter of minutes. Rate is greater than remove the unit before cardioversion since the
300 beats per minute electric shock may damage the unit
10. Avoid direct application of electric shock on pace 8. If necessary prepare to defibrillate a second time,
makers if present. using 300 joules of energy.
11. Place the client in a flat and firm surface and 9. If defibrillaton is once again necessary, defibrillate
apply interface material to the paddles for the 3rd time using 360 joules of energy
12. Give command for personnel to STAND CLEAR 10. In documenting defibrillation, do not forget to
of the client and the bed chart: that the procedure was performed, patient’s
13. Apply chest paddles as follows: one at the right of ECG rhythm before and after the procedure, number
the sternum, third ICS; and the other on the left mid of times defibrillation was performed, voltage used
axillary fifth ICS during each attempt, whether a pulse returned,
14. Push the discharge button on paddles dosage, route and time of drug administration,
simultaneously whether CPR was done, means of airway
maintenance and patient’s outcome.

DEFIBRILLATION PACEMAKERS

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 TRANSCUTANEOUS PACEMAKERS
effects of fibrillation is highly dependent on quick A temporary form of pacemakers
and early identification of the arrhythmia. The device works by sending electrical impulses
from the pulse generator to the patient’s heart by way
Mechanism: of two electrodes, which are placed on the back and
The current delivered by defibrillation causes the the front of the patient’s chest.
myocardium to depolarize, which in turn encourages Used only until the doctor can institute transvenous
the sinoatrial node to resume control over the heart’s pacing
electrical activity.
TRANSVENOUS PACEMAKERS
More reliable compared to that of your
Nursing Responsibilities: transcutaneous pacemakers
1. Assess the patient if he lacks pulse. Call for help Involves threading an electrode catheter into the
and immediately perform CPR until the defibrillator cephalic or jugular vein into the patient’s right atrium
and other emergency equipments arrive or right ventricle
2. Expose the client’s chest and apply conductive The electrode then attaches to an external pulse
pads at the paddle placement positions or apply gels generator
to the paddles. Place one paddle at the right of the The pulse generator can directly initiate impulse
upper sternum, just below the clavicle and the other towards the myocardium
over the fifth or sixth intercostal space at the left
anterior axillary line. PERMANENT PACEMAKER INSERTION
3. Turn on the defibrillator and set the energy level at A self contained device designed to last for 3-20
200 joules for an adult person years. The surgeon implants the pacemaker beneath
4. Place the paddles over the conductive pads (if the client’s skin
used), and press firmly applying 11 kg of pressure Today, Permanent Pacemakers function in a demand
5. Instruct all personnel to stand clear of the patient mode, allowing the patients heart to function on its
and the bed own while preventing it from falling to a preset rate
6. Discharge the current by pressing both paddle
charge buttons simultaneously Nursing Responsibilities:
7. Reassess the client’s cardiac rhythm and have 1. Clean incision site with soap and water
someone else assess the client’s pulse
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 o If BP cuff is used as
contract more effectively by tourniquet, inflate BP up
improving the contractile force of to 10-40 mmHg more than
the muscle the diastolic pressure
• Examples : Digoxin, Dopamine o Perform neurovascular
(Intropin), Dobutamine (Dobutrex) check distal to the
and Milrinone (Primacore) tourniquet : Pallor,
Amrnone (Inocore) Paresthesia,
3. Vasodilator Therapy Poikilothermia, Pain
• Decreases the workload of the heart o Avoid too tight tourniquet
by dilating the peripheral vessels. application as ischemia
This decreases ventricular preload may occur
and volumes
• Examples: Nitrates
(Nitroglycerine), Hydralazine Nursing Management:
(Apresoline), Prazosin (Minipress),
Sodium Nitroprusside (Nipride), A. Maintaining Adequate Cardiac Output and
Morphine Sulfate (Dura Morph) Improving Circulation
4. Angiotensin-Converting Enzyme a. Place patient at physical and
Inhibitors (ACE Inhibitors) emotional rest in order to reduce
• Inhibits the vasoconstricting work of the heart
capacity of the ACE b. Place client in semi recumbent
• Decreases left ventricular afterload position in an air conditioned
with a subsequent decrease in heart environment
rate thereby reducing cardiac c. Provide bedside commode
workload d. Provide psychological rest by
• Examples: Captopril (Capoten), promoting physical comfort, avoid
Enalapril (Vasotec) anxiety
7. Beta adrenergic Blocking Agents (Beta e. Monitor for progression of left
Blockers) ventricular failure
• Blocks the sympathetic effects of i. Observe lowering systolic
epinephrine and norepinephrine on blood pressure, and
the heart narrowing pulse pressure
• Examples: Selective: Metoprolol ii. Note for alternations of
(Lopressor) non-selectove: weak and strong pulses
Carvedilol iii. Auscultate and Monitor
8. Diet for S3 gallop and S4
sounds : common in CHF
• Low sodium with fluid restrictions
iv. Monitor for premature
9. Surgery
ventricular beats
• Heart Transplant
• Phlebotomy f. Monitor for signs of poor systemic
o Dry phlebotomy or circulation
rotating tourniquets g. Administer pharmacotherapy as
intends to allow pooling of ordered
blood in the lower h. Supports lower arms with pillows
extremities, thereby i. Auscultate lung fields every four
reducing preload hours for presence of crackles and
o Three extremities are wheezes
occluded at a time j. Change position of client
o Rotate tourniquets frequently every 2 hours
clockwise every k. Encourage deep breathing exercises
15minutes; each extremity l. Offer small frequent feedings to
is occluded for a prevent overdistention of stomach
maximum of 45 minutes reducing space for lung expansion
m. Administer oxygen as directed activity without discomfort. Symptoms
occur even at rest.
B. Restoring Fluid Balance
a. Administer prescribed diuretics and
give it AM Therapeutic Classifications of Patients with Heart
b. Input and Output recording must be Diseases:
initiated
c. Weigh patient daily Class A: Patients with cardiac disease
d. Give oral potassium as prescribed whose ordinary physical activity need not be
if taking Loop diuretics restricted
e. Observe for signs of electrolyte
depletion : lassitude, apathy, mental Class B: Patients with cardiac disease
confusion, anorexia, decreasing whose ordinary physical activity need not be
urinary output restricted but should be advised against
f. Limit Oral Fluid Intake as well as severe or competitive physical efforts
IV infusions
g. Monitor for pitting edema on lower Class C: Patients with cardiac disease
extremities and sacral area. Use egg whose ordinary physical activity must be
crate mattress and sheep skin to moderately restricted and whose more
prevent pressure soars strenuous efforts should be discontinued
h. Be alert for complains of right
upper quadrant pain. May indicate Class D: Patients with cardiac disease
liver congestion whose ordinary physical activity should be
i. Avoid salt in diet markedly restricted

C. Improving Activity Intolerance Class E: Patients with cardiac disease who


a. Improve patient’s activity gradually should be at complete bed rest, confined to
according to limitations bed or chair.
b. Frequently monitor patient’s heart
rate during activity and be alert for
complains of chest pain or skeletal
pain VALVULAR DEFECTS
c. Relieve for night time anxiety and
provide rest and sleep
The function of normal heart valves is to maintain the
Functional Capacity Classification of Patients forward flow of blood from the atria to the ventricles
with Heart Diseases: and from the ventricles to the great vessels.

Class I: Patients with cardiac disease but Valvular damage may interfere with valvular
with no limitations of physical activity. function by stenosis or by impaired closure that
allows backward leakage of blood (valvular
Class II: Patents with cardiac disease but insufficiency, regurgitation and incompetence).
with slight limitations of physical activity.
Comfortable at rest. Ordinary physical
activity results in fatigue, palpitations, Mitral Stenosis
dyspnea and or angina
Progressive thickening and contracture of
Class III : Patients with cardiac disease valve cusps with narrowing of the orifice and
resulting in marked limitation of physical progressive obstruction to blood flow. The left atrium
activity. They are comfortable at rest. Less has difficulty in emptying itself into the left ventricle,
than ordinary physical activity causes therefore it dilates and hypertrophies. As a result of
symptoms. the abnormally high pulmonary arterial pressure that
must be maintained, the right ventricle is subjected to
Class IV: Patients with cardiac disease a pressure overload and may eventually fail.
resulting in inability to carry on any physical
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 a. Assess frequently for presence of
b. Dyspnea, cough, orthopnea, murmurs
nocturnal dyspnea and murmurs b. Assess for signs of let and/or right
c. Dysrhythmia, palpitations ventricular failure
d. Hemoptysis c. Monitor and treat dysrhythmias as
e. Low blood pressure, dizziness, ordered
syncope, angina, symptoms of CHF d. Prepare patient for surgical
f. Neck vein distention and visible operation
and palpable arterial pulsations
over the precordium B. Improving Tolerance
a. Maintain bedrest until symptoms of
Diagnostic Evaluation: CHF are present
a. Echocardiography may show b. Allow patient to rest between
abnormalities of valve structure and interventions
chamber size and thickness c. Begin activities gradually as
b. Chest X-ray shoes signs of tolerated
cardiomegaly and pulmonary vascular d. Assist or perform hygiene needs
congestion and other needs of the client
c. Cardiac catheterization and
angiocardiography 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)