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CARDIAC DISORDERS

- Generic term for disorders of heart and blood vessels


- Disorders of Myocardial perfusion --------Oxygenation
 Coronary Artery Disease
 Angina Pectoris
 Acute Myocardial Infarction
 Cardiac Dysrthythmia
 Sudden Cardiac Death

1. Review of Anatomy and Physiology of the Cardiovascular System


THE HEART: ITS STRUCTURE AND FUNCTION
STRUCTURE FUNCTION
Pericardium Two-layered sac that encases and protects the heart
Atrium Upper, receiving chambers of the heart
• Right Atrium Receives deoxygenated systemic blood via superior and
inferior vena cava; blood passes to right ventricle
• Left Atrium Receives oxygenated blood from the lungs; blood passes
to the left ventricle
Ventricles Lower, pumping chambers of the heart
• Right ventricle Receives blood from atrium via the tricuspid valve;
pumps it to the pulmonary circulation
• Left Ventricles Receives blood from atrium via the bicuspid (mitral
valve); pumps it to the systemic circulation
Cardiac Valves Prevent backflow of blood
• Atrioventricular Prevent backflow from right atrium (tricuspid valve) and
valves from left ventricle to left atrium (mitral valve)
• Semilunar Prevent backflow from pulmonary artery to right
valves ventricle (pulmonic valve) and from aorta to left
ventricle (aortic valve)
Coronary Arteries Provide blood supply to the heart
• Right coronary Profuse right atrium, right ventricle, inferior portion of
artery the left ventricle and posterior septal wall, SA node , AV
• Left Coronary node
Artery:
- Left anterior
descending Supplies blood to anterior wall of left ventricle, anterior
artery ventricular septum, and apex of the left ventricle
- Circumflex
artery Provides blood to left atrium, lateral and posterior
surfaces of the left ventricle, occasionally the posterior
intraventricular septum
SA node “pacemaker” node, initiates heartbeat by generating an
electrical impulse
AV node Normal pathway for impulses originating in the atria to
be conducted to ventricles; can be a secondary
pacemaker
Bundle of His, bundle Rapidly transmit cardiac action potentials to enable
branches, Purkinje’s synchronous contraction of ventricles
fiber

Electrophysiologic Properties of the heart


♥ Excitability- ability of the heart to respond to an electrical impulse
♥ Automaticity- ability to initiate an electrical impulse
♥ Conductivity- ability to transmit an electrical impulse from one cell to
another
♥ Contractility- force exerted for heart to contract
♥ Refractoriness- ability to respond to new stimulus

CARDIAC ACTION POTENTIAL


5 PHASES:
I. Phase 0 : cellular depolarization is initiated as positive ions influx into the cell
II. Phase 1 : Early cellular repolarization begins during this phase as potassium
exits the intracellular space
III. Phase 2: This phase is called the plateau phase because the rate of
repolarization slows. Ca+ enters the intracellular space
IV. Phase 3: completion of repolarization and return of the cell to its resting state
V. Phase 4: resting phase before the next depolarization

Cardiac Output
♥ Volume of blood ejected/min by rhythmic ventricular contraction
o CO= Stroke Volume x HR
o Averages between 4-8L/min in adults
♥ Stoke volume has a major influence on cardiac output
o Preload
o Afterload
o Contractile state of the heart
♥ Heart rate

Autonomic Nervous System and the Heart


♥ Parasympathetic nerve activity
♥ Sympathetic nerve activity
♥ Adrenergic receptor stimulation
o Alpha1 adrenergic receptors
o Alpha2 adrenergic receptors
o Beta1 adrenergic receptors
o Beta2 adrenergic receptors

ASSESSMENT OF THE CARDIAC SYSTEM

History
• Note risk factors
o Non-modifiable risk factors
o Modifiable risk factors
• Symptom Analysis
o Dyspnea
 Dyspnea on exertion
 Orthopnea
 Paroxysmal nocturnal dyspnea
o Chest pain
o Palpitations
o Syncope
o Fatigue
o Weight gain and dependent edema

Physical Examination
 Inspection
o General Apperance
o Level of Consciousness
o Skin
 Color
 Turgor
 Edema
o Fingers
• Capillary refill
• Clubbing
o Neck
• Neck vein distention
o Chest
• Symmetry
• Respiratory rate and effort
o Tachypnea
o Cheyne-strokes respirations
o Hemoptysis
o cough
 Palpation
o Peripheral pulses
o Apical pulse
o Abdomen
 Liver enlargement (hepatojugular reflux)
 Ascites
 Bladder distention
 Auscultation
o Blood pressure
 Pulsus paradoxus
o Heart sounds
• Normal heart sounds (S1 and S2)
• Gallops (S3 and S4)
• Clicks
• Precordial friction rub
• Murmurs (location, timing, intensity, pitch, quality,
radiation)
o Breath sounds
• Crackles
• Wheezes

Diagnostic Test and Procedures

A. Non-Invasive
 Electrocardiography
o Holter monitoring
o Stress testing
 Echocardiogram
 Ultrasound
 Chest X-ray
 Radionuclide studies
 Magnetic Resonance Imaging (MRI)
 Positron emission tomography (PET)

B. Invasive
 Cardiac catheterization
 Arteriogram
 Angiocardiogram
 Venogram
 Lymohography
 Bone Marrow Aspiration
 Myocardial Scintigraphy
o Thalium 201
o Technetium 99m

C. Laboratory Test
 BLOOD CHEMISTRIES
o Sodium
o Potassium
o Calcium
o Magnesium
o Blood Urea Nitrogen (BUN)
o Phosphorus
 COAGULATION STUDIES
o Partial thromboplastin time
o Activated partial thromboplastin time
o Prothrombin time
o Internal normalized ratio
 HEMATOLOGIC STUDIES
o CBC
o WBC
o Hemoglobin and hematocrit
o Platelets
 Serum Lipids
o Cholesterol
o Triglycerides
 Cardiac enzymes
o Myoglobin
o Creatinine kinase (CK)
o Lactic acid dehydrogenase (LDH)
o Troponin 1
o Aspartate aminotransferase (AST)
 Hemodynamic Studies
o Pulmonary artery catheter

PEDIATRIC CARDIOVASCULAR DISORDERS


1. Congenital Heart Disease
- Involve all chambers, valves and great vessels arising from the heart
- In most cases, the cause is unknown; some infants and children with
CHD may appear perfectly healthy while others may be critically ill
- Most can be successfully managed with medications and surgery
- Associated factors of CHD include:
 Fetal or maternal infection during the first trimester (rubella)
 Chromosomal abnormalities (Trisomy 21, 18, 13)
 Maternal insulin-dependent diabetes
 Teratogenic effect of drugs and alcohol

Common Congenital Heart Malformations


• Obstructive lesions
- Aortic valve stenosis
- Coarctation of the aorta
- Pulmonary valve stenosis
• Increased pulmonary blood flow (acyanotic)
- Patent ductus arteriosus
- Atrial septal defect
- Ventricular septal defect
- Atrioventricular canal
• Decreased pulmonary blood flow (cyanotic)
- Tetralogy of Fallot
- Tricuspid atresia
- Total anomalous pulmonary venous return
- Transposition of great arteries
- Truncus arteriosus
- Hypoplastic left heart syndrome

Diagnostic Evaluation
• Auscultation: murmur (except on TGA), ejection click (especially on AOS
and PS), single S2
• ECG: left ventricular hypertrophy
• CXR: increased cardiac silhouette
• Echocardiogram

2. Aortic Valve Stenosis


• May be used a bicuspid aortic valve with fused commissures that does not
open completely
• Results in a turbulent blood flow across the aortic valve and into the
ascending aorta; left ventricular pressure must rise to overcome the
increased resistance
• Myocardial ischemia may occur because of an imbalance between the
increased oxygen requirements related to the hypertrophied left ventricle
and the amount of oxygen that can be supplied
• Left ventricular failure may result

Clinical Manifestations
NEWBORN WITH CRITICAL AORTIC STENOSIS
 Severe congestive heart failure
 Metabolic acidosis
 Tachypnea
 Faint peripheral pulses, poor perfusion, poor capillary refill,
cool skin
 Poor feeding
CHILD AND ADOLESCENT
 Chest pain on exertion, decreased exercise tolerance
 Dyspnea, fatigue, SOB
 Syncope, lightheadedness
 Palpitation
 Sudden death

Management:
• Stabilize with prostaglandin E1 infusion to maintain CO
• Inotropic support
• Intubation and ventilation as needed
• Restrict intense and anaerobic exercise
• Cardiac catheterization: aortic balloon valvotomy

3. COARCTATION OF THE AORTA


- Discrete narrowing of a long segment hypoplasia of the aortic arch,
usually distal to the left subclavian artery, increasing the workload of
the left ventricle

Clinical Manifestations
 Newborn with critical COA
o Asymptomatic until PDA begins to close
o After PDA closure: severe CHF, poor perfusion,
tachypnea, acidosis, absent femoral pulses
 Child or adolescent with COA
• Usually aymptomatic
• Hypertension in the upper extremities, with absent or
weak femoral pulses
• Nosebleeds, headaches, leg cramps
Management
- Stabilize with prostaglandin E1 infusion to maintain CO
- Inotropic support
- Intubation and ventilation as needed
- Assess renal, hepatic, and neurological function
- Surgical intervention: subclavian flap repair (Waldhausen procedure)
4. PATENT DUCTUS ARTERIOSUS
- When the ductus arteriosus fails to close, blood from the aorta (high
pressure) flows into the pulmonary artery (low pressure), resulting in
pulmonary artery (low pressure), resulting in pulmonary overcirculation
- Increased pulmonary blood flow leads to a volume loaded LV

CLINICAL PRESENTATION
• Small to moderate-size PDA
 Usually asymptomatic
• Large PDA
 CHF, tachypnea
 Poor weight gain, failure to thrive
 Feeding difficulties
 Decreased exercise tolerance

Management
• Monitor growth and development
• Increase caloric intake for normal weight gain
• Indomethacin and diuretics
• Caridac Catheterization
• Surgical intervention: PDA ligation via lateral thoracotomy

5. ATRIAL SEPTAL DEFECT


- An abnormal communication between left and right atria
- There are three types
o Ostium secundum ASD: opening in the middle of the septum
o Ostium primum ASD: opening at the bottom of the septum
o Sinus venosus ASD: opening at the top of the septum
- Blood flows from the higher-pressure left atrium across the ASD into
the lower-pressure right atrium, increasing blood return to the right
heart leading to RV hypertrophy

Clinical Manifestations
• Ostium secundum and sinus venosus are usually are usually
asymptomatic
• Ostium primum ASD
o CHF
o Frequent URTI
o Poor weight gain
o Decreased exercise tolerance
Management
 Monitor and reassess small spontaneous closure rate
 Surgical Intervention
• Primary repair: suture closure of the ASD
• Pericardial patch repair of the ASD

6. VENTRICULAR SEPTAL DEFECT


- Abnormal communication between the right and left ventricles
- VSDs vary in the size (small and restrictive to large and nonrestrictive
defect), number (single versus multiple), and type (perimembranous or
muscular)
- Blood flow from the high-pressure LV across the VSD into the low-
pressure RV and into the pulmonary artery (left-to-right shunt),
resulting in pulmonary over circulation, increase pulmonary venous
return, left atrial dilation
- Long-standing pulmonary over circulation causes increase pulmonary
vascular resistance, which then could reverse the blood flow pattern to
right-to-left shunt across the VSD (Eisenmenger’s syndrome), resulting
in cyanosis

Clinical Manifestations:
 Small VSDs
• Usually asymptomatic
• High spontaneous closure rate during the first year of
life
 Large VSDs
• Tachypnea, tachycardia, excessive sweating
associated with feeding, hepatomegaly
• Frequent URTI
• Poor weight gain, failure to thrive
• Feeding difficulties

Management:
 CHF management with digoxin and diuretics
 Avoid O2; O2 is a potent pulmonary vasodilator and will
increase blood flow into pulmonary artery
 Increase caloric intake
 Surgical intervention: patch closure VSD

7. TETRALOGY OF FALLOT
- Most common complex congenital heart defect which include four
abnormalities
 A large nonrestrictive VSD
 Aortic override
 Right ventricular outflow tract obstruction
 Right ventricular hypertrophy
- Degree of cyanosis depends on the size of the VSD and the degree of
RVOTO
- Obstruction of blood flow from the LV to the pulmonary artery results
in deoxygenated blood being shunted across the VSD and into the
aorta resulting in cyanosis
- Minimal right ventricular outflow tract obstruction results in a pink TOF
variant

Clinical Manifestations
 Variable and depend on the size of the VSD and degree of
RVOTO
 Cyanosis
o Cyanosis may initially be observed only with crying
and with exertion
 Polycythemia
 Squatting
o A posture characteristically assumed by older children
to increase systemic vascular resistance and to
encourage increase pulmonary blood flow
 Tet Spell
o A life threatening hypoxic event with a dramatic
decrease in O2 saturations
o Typically occur in the morning soon after awakening,
during or after a crying episode, during painful
procedures
o Includes tachypnea, irritability, and increased
cyanosis, followed by flaccidity and loss of
consciousness
o Usually prompt cardiologist to refer for surgical
intervention

Management
- Monitor O2 saturation, growth and development, hypoxic spells
- Surgical intervention
o Palliative: modified Blalock-Taussig shunt; tube graft between
the left subclavian artery and pulmonary artery
o Definitive: patch closure of VSD, relief of RVOTO

8. Transposition of the Great Arteries


• Occurs when pulmonary arteries arises off the left ventricle and the aorta
arises of the right ventricle
• The defect results in two parallel circulations
• To sustain life, there must be an accompanying defect that allow mixing of
deoxygenated blood and oxygenated blood between two circuits
Clinical Manifestations
 Symptoms evident soon after birth
o Cyanosis
o Tachypnea
o Metabolic acidosis
Management
- Stabilize with prostaglandin E1 infusion to maintain CO
- Balloon atrial septostomy to improve atrial level mixing
- Treat pulmonary over circulation with diuretics
- Surgical intervention
o Arterial switch operation (Jatene)
o Rastelli operation

9. TRICUSPID ATRESIA
- There is no communication between the right atrium and right
ventricle
- Associated lesions include
o Obligatory of PFO or ASD
o PDA
o VSD
o Hypoplastic RV
- With TA systemic venous return enters the right atrium and cannot
continue into the RV; flows across an atrial septal opening into the left
atrium

Clinical Manifestation
 Cyanosis
Management
• Stabilize with prostaglandin E1 infusion to maintain CO
• Intubation and ventilation as needed
• Surgical intervention

10. HYPOPLASTIC LEFT HEART SYNDROME


- A constellation of left heart abnormalities that include the following
o Critical mitral stenosis or atresia
o Hypoplastic LV
o Critical aortic stenosis or atresia
o Hypoplastic ascending aorsat with severe coarction of the aorta
- The left side of the heart is underdeveloped and essentially
nonfunctional
- RV supports both the pulmonary and systemic circulations
- ASD allows blood to flow from the left atrium into the right heart and
blood flows right to left across the PDA and into the descending aorta
to deliver O2 and nutrients

Clinical Manifestations
 Newborn may appear completely well
 Once PDA begins to close
o CHF and tachypnea
o Decreased urine output
o Poor feeding
o Lethargic, change LOC
o Pallor; gray color
o Weak peripheral pulses

Management
 Stabilize with prostaglandin E1 infusion to maintain CO
 Inotropic support
 Balloon atrial septostomy to improve atrial level mixing
 Assess hepatic, renal and neurological function
 Surgical intervention: cardiac transplantation

Nursing Care to clients with Congenital Heart Disease


1. Assessment
o Height and weight
o Vital signs and O2 saturations
o Skin color, mucous membranes and extremities
o Clubbing
o Respiratory pattern, heart sounds , fluids status and
level of activity
2. Relieve respiratory distress
o Position in reclining, semi-upright position
o Suction oral and nasal secretion as needed
o O2 as prescribed
3. Improve Oxygenation and Activity tolerance
4. Provide adequate nutrition

11. Acute Rheumatic Fever


- Acute autoimmune disease that occurs as a result group A beta
hemolytic streptococcal infection
- Characterized by inflammatory lesions and of connective tissue and
endothelial tissue, primarily affecting the joints and heart
- Most occur 2 to 3 weeks after a strep infection of the throat or URTI
- Infection abates with or without treatment; however autoantibodies
attack the myocardium, pericardium and cardiac valves
o Aschoff bodies lead to permanent valve dysfunction
o Severe myocarditis may cause dilation of the heart and failure

Clinical Manifestations (Jones Criteria)


Major Manifestations
 Carditis
• Systolic murmur, prolong PR and QT intervals, possible signs of HF
 Polyarthritis
• Pain and limited movement of two or more joints; joints are swollen, red,
warm and tender
 Chorea
• Involvement of the nervous system
• Sudden, purposeless, involuntary, rapid movements often associated with
muscle weakness, involuntary facial grimace, speech disturbance and
emotional lability
 Erythema marginatum
• Non-pruritic pink, macular rash mostly of the trunk with pale central areas
 Subcutaneous nodules
• Firm, painless nodules over the scalp and extensor surface of joints

Minor Manifestations
 History of previous rheumatic fever or evidence of
preexisting rheumatic heart disease
 Arthralgia
 Fever
 Laboratory abnormalities
o Elevated ESR and WBC
o Positive C-reactive protein
 ECG changes
• Prolonged PR interval

Diagnostic Evaluation
 ECG
 ASO titer
 CXR
Collaborative Management
 Antibiotic therapy
o Benzathine penicillin IM
o Oral Erythromycin
 NSAIDs for pain relief and control cardiac inflammation
 Corticosteroid in severe cases to control cardiac inflammation
 Salicylates to control fever
 Phenobarbital and Diazepam for chorea
 Bed rest to maintain optimal cardiac function

Nursing Care
- Improved cardiac output
o Explain need for bed rest
o Light indoor activity
o Organize care for uninterrupted
- Relieve pain
o Administer NSAIDs as prescribed
o Watch out for toxicity of meds
o Assist to comfortable position
- Protect the child with chorea
o Use padded side rails
o Assist with feeding and other fine motor activities
o Offer emotional support

12. KAWASAKI DISEASE


- Mucocutaneous lymph node syndrome
- Multisystem vasculitis identified by a febrile illness with features that
compromise vital body systems
- Cause is unknown, although exposure to retrovirus, Proprionibacteriae
and Group A streptococcus have been implicated
- Cardiovascular system seems to be primarily involved
- Major Mannifestations= tongue redness

Clinical Manifestations
 Acute febrile phase- Stage 1
o Child appears severely ill and irritable
o High, spiking fever to 5 more days
o Bilateral conjuctival infection
o Oropharyngeal erythema
 “strawberry” tongue
 Red and dry lips
o Indurative edema of hands and feet, erythema of palms and soles,
general edema, or periungal desquamation (cracked hands or sole)
o Erythematous rash
o Cervical lymphadenopathy
o Carditis
Pericarditis and myocarditis
Cardiomegaly, CHF, and pleural effusion
Iridocyclitis (redness of the sclera) and aseptic meningitis, dry
cracked lips with fissures
 Sub-acute phase- Stage II
o Acute symptoms of stage 1 subside as temp returns to normal
o Child remains irritable and anorectic
o Dry, cracked lips with fissures
o Desquamation of toes and fingers
o Arthralgia and arthritis
o Coronary thrombosis, aneurysms
 Convalescent phase- Stage III
o Child appears well
o Transverse grooves of fingers and toenails (Beau’s line)
o Coronary thrombosis, aneurysms
 Stage IV
o Coronary artery scaring (due to frequent vasculitis, scarring occurs),
stenosis and calcification
o Myocardial fibrosis(hardening) and endocardial fibroelastosis (loss of
elasticity)
o Healing begins

Diagnostic Evaluation
 The CDC requires that fever and four of the other criteria listed above in
stage I be demonstrated
 ECG, echocardiogram, cardiac catheterization and angiocardiography may be
required to diagnosed cardiac abnormalities
 To help support the diagnosis and rule out other diseases
o CBC: leukocytosis during acute stage
o ESR: elevated during acute stage
o RBC and hemoglobin : slight decrease
o C-reactive protein: positive
o Platelet count: increased during 2nd to 4th week of illness
o IgM, IgA, IgG: transiently elevated
o Urine: Protein and leukocytes present
o Elevated transaminase (liver enzymes)
 Collaborative Management
o Single dose of IVGG during stage 1 (Intravenous Gamma Globulin to help
boost the immune system of the child.
o Aspirin Therapy
 Anti-inflammatory
 Antiplatelet
o Thrombolytic therapy (ex. Strrptokinase)
o Supprotive measures
 Maintain fluid and electrolyte balance and nutrition
 Provide comfort
Nursing Care:
 Allow child of uninterrupted rest
 Offer pain relief
 Perform comfort measures related to the eye
o Darken the room and offer sunglasses
o Apply cool compress
o Discourage rubbing of eyes or place mittens (gloves)
to children
 Perform comfort measures related to joint pain and tender
lymph nodes
o Use PROM every 4 hours (PROM)
o Allow and encourage to move freely
 Provide quite, peaceful environment with diversional
activities
 Maintain cardiac output
 Take V/S and monitor for CHF
 Preserving oral mucous membrane
 Offer and encourage cool liquids
 Progress to soft, bland foods
 Give mouth care (warm gargle; no strong mouth wash!)
 Improve skin integrity
 Avoid using soap that tends to dry the skin
 Elevate edematous extremity (promote early venous return)
 Use egg-crate mattress (to avoid bed sores)
 Maintaining fluid balance
 Offer clear liquids
 Monitor hydration status (thru skin turgor and sunken
fontanel for infants)
 Reduce fear
 Use play therapy
 Practice relaxation technique with child
I. Disorders of Myocardial Perfusion
A. CORONARY ARTERY DISEASE OR CORONARY HEART DISEASE

- Heart disease caused by impaired blood flow to myocardium


- Cause is accumulation of atherosclerotic plaque in coronary arteries
(blood supply of heart)
- May be asymptomatic or cause angina pectoris, MI (heart attack),
dysrhythmias, heart, failure, sudden death

Major Risk Factors:


• Non-modifiable
 Heredity
 Increasing age
 Gender
• Modifiable
 Smoking
 Hypertension
 Elevated serum cholesterol levels
 Physical inactivity
 Obesity
 Diabetes
• Contributing Factors
 Response to stress
 Homocysteine levels (treatment of folic acid—Vit B6)
 Menopause

Pathophysiology
 Progressive disease characterized by atheroma (plaque formation)
 Affecting intimal and medial layers and medium sized arteries
 Initiated by unknown precipitating factors that cause lipoproteins and fibrous
tissue to accumulate in arterial wall
 Begins with injury or inflammation of endothelial cells lining artery promoting
platelet adhesion and aggregation, WBCs go to area
 At injury site, lipoproteins collect in intimal lining contact with platelet,
cholesterol, blood components stimulate smooth muscle cells and connective
tissue to proliferate within vessel wall
 Fibrous plaque develops and blood lipids accumulate
 Developing plaque gradually occludes vessel lumen and impairs ability of
vessel to dilate; occurs at bifurcations, curves, narrowed areas
 Plaque expands to create stenosis or total occlusion of artery
 Development of atheromas which become calcified and can ulcerate or
rupture, stimulating thrombosis; can be occluded by thrombus or can
embolize to distal vessel
 Manifestations of process do not appear unitl 75% lumen occluded

Clinical Manifestations:
 Rapid progression may cause ischemia resulting in unstable
angina, MI and sudden cardiac death
 Slow progression is associated with chronic stable angina

Collaborative Management
- Reduce risk factors (by patient himself through change in lifestyle)
- Restore blood supply
o Percutaneous Transluminal Coronary Angioplasty (PTCA)
o Directional Coronary atherectomy
o Intracoronary stents and laser ablation ( breaks down the coronary
clots)

- Surgical Intervention
o Coronary Artery Bypass Graft (CABG)
o Transmyocardial Revascularization
- Medical Management
o Antiplatelet
o Antilipemics (Anticholesterol--- ex. Simvastatin)

Nursing Care
 Reduce risk factors
o Daily management of hypertension
o Smoking cessation
o Avoid passive smoke
o Plan regular exercise
o Maintain ideal body weight
o Follow a healthy diet
 Reduce cholesterol
 Increase fiber

B. ANGINA PECTORIS
 Transient chest pain resulting from reduced coronary blood flow causing a
temporary imbalance between myocardial blood supply and demand
 Due to CAD, atherosclerosis or vessel constriction that impairs blood supply
to myocardium
Pathophysiology
 Temporary and reversible myocardial ischemia caused by partial obstruction
of coronary artery, coronary artery spasm or thrombus
 Cells in region supplied by artery are deprived of essential O2 and nutrients
for metabolic processes compromising cellular processes
 Cells switch to anaerobic metabolism causing lactic acid to build up in cells
 Cell membranes release histamine, kinins, specific enzymes stimulating
nerve fibers in cardiac muscle that send pain impulses to CNS
 Pain radiates to upper body because heart shares same dermatome as this
region
 Return of adequate circulation provides nutrients and clears away waste
products
 More 30 mins. Of ischemia irreversible damages myocardial cells or necrosis

Characteristics of Angina
• Onset
o Can develop quickly or slowly
o Precipitated by activity
• Location
o Retrosternal or slightly to the left of the sternum
• Radiation
o Usually radiates to the left shoulder and upper arm and may then
travel down the inner aspect of the left arm to the elbow and wrist
• Duration
o Lasts less than five minutes
o Attacks precipitated by heavy meal or extreme anger may last 15-
20minutes
• Sensation
o Pain as squeezing, burning, pressing, choking, aching, bursting
pressure
o Pain feels like gas, heartburn or indigestion
• Severity
o Pain is mild to moderate
• Associated characteristics
o Dyspnea
o Pallor
o Sweating
o Faintness
o Palpitations
o Dizziness
o GI disturbances
• Atypical Presentation
o In women, may be manifested by epigastric pain, dyspnea or back
pain
o In elderly, frequently experiences dyspnea, fatigue or syncope
• Relieving or aggravating factors
o Aggravated by continued activity
o Typical “exertion-pain, rest-relief” pattern
• Treatment
o Should subside after nitroglycerine

Patterns of Angina
 Stable Angina
• Paroxysmal chest pain or discomfort triggered by a predictable degree of
exertion or emotion
 Unstable Angina
• Preinfaction angina, crescendo angina, intermittent coronary syndrome
• Paroxysmal chest pain triggered by an unpredictable degree of exertion of
emotion
 Variant Angina
• Prinzmetal’s angina
• Similar to classic angina but of no longer duration
 Nocturnal angina
• Possibly associated with REM sleep
 Angina decubitus
• Paroxysmal chest pain that occurs when the client reclines and lessens
when the client sits or stands up
 Intractable Angina
• Chronic incapacitating angina that is unresponsive to intervention
 Post-Infarction angina
• Pain occurs after MI

Diagnostic Evaluation
 Electrocardiography
 Exercise ECG
 Radioisotope imaging
 Electron-Beam Computed Tomography
 Coronary Angiography

Collaborative Management
 Relieve acute attack
o Opiate analgesics
o Vasodilator
 Nitroglycerine
 Isosorbide
o Beta-Adrenergic Blockers
o Calcium-Channel blockers
o Antiplatelet agents

Nursing Care
 Promote comfort
 Promote tissue perfusion
 Encourage activity and rest
 Facilitate Learning
o Avoid 4 E’s
 Eating heavy meals, drinking coffee and smoking
 Extreme temperature like cold weather
 Excessive stress and emotion
 Exercising strenuously
o Weight reduction and IBW maintenance
 Promote relief of anxiety and feeling of well-being

C. ACUTE MYOCARDIAL INFARCTION


- Formation of localized necrotic area within the myocardium
- Usually caused by sudden coronary occlusion and abrupt cessation of
blood and O2 flow to the heart muscles
- Partial occlusion can lead to development of ischemic zone (reversible
if O2 is given immediately)
- Total and prolonged occlusion more than 35-45 minutes would lead to
zones of injury and infarction which produces irreversible cellular
damage and necrosis to the myocardium (contractile function ceases)

Areas of the heart


 Particular coronary artery occluded determines area of damage
 The specific infarct site predicts possible complications and dictates possible
complications and dictates possible therapy
 Specific artery and area affected
o Left anterior descending artery (LADA) (most common)- damages left
ventricle causing anterior wall infarct
o Left circumflex artery (LCA)- lateral MI
o Right coronary artery (RCA) and posterior descending artery (PDA)-
right ventricular, inferior and posterior infarct
o Left main coronary artery –entire left ventricle and a grave prognosis
Depth of infarction in the ventricular wall
 Subendocardial
o Damage is limited to subendocardial tissues
o Occurs within 20 minutes of injury
 Intramural
o Associated with long standing angina pectoris
 Subepicardial
o Damage is limited to subepicardial tissues
 Transmural
o Damage extends through all 3 layers
o Most common complication is heart failure
 Cocaine intoxication can cause acute MI secondary to sympathetic nervous
system stimulation resulting in over-stimulation of the heart, dysrhythmias
and vasoconstriction

Clinical Manifestations of AMI:


 Pain! (Classic manifestation)
o Crushing, severe, prolonged chest pain
o Lasts > 15-20 minutes
o Onset sudden and usually not associated with activity
o Unrelieved by rest or nitroglycerine
o Substernal pain may radiate to the neck, jaw, shoulders, both arms,
back, epigastrium
o Characterized by Levine’s sign
o Women and older adults have atypical chest pain with complaints of
indigestion, heartburn, nausea, vomiting
o No chest discomfort in 25% of clients with acute MI
 Anxiety and apprehension
o Feeling of impending doom
o Restlessness results from shock and pain
 SOB, dyspnea and dizziness
 “indigestion”, nausea and vomiting
 Palpitation, cold sweat and paleness
 ECG changes
o Pathologic Q wave enlargement (area of infarction)
o T wave inversion (zone of ischemia)
o ST segment elevation (zone of injury)- usually occurs as an initial
change in AMI
 Elevated intracellular enzymes
o Myoglobin
 May increase in heavy ethanol use, strenuous exercise and
damage to myocardial tissues
 Increase within 2 hours ends in 24 hours
o CK-MB
 Most definitive finding in MI, especially in the presence of
increased levels of LDH
 Increase 3-6 hours after, peak 12-18
o Troponin I
 Very specific and sensitive indicator of AMI because not
affected by other diseases
 Increase 7-14 hours after injury up to 5-7 days
o LDH
 Release when myocardial damage occurs
 Increase 14-24 hours after, peaks 48-72 hours
o AST
 Increase several hours after, peaks 48-72 hours
 Imaging
o PET
 Visualizes cardiac metabolism and tissue perfusion
o MRI
 To show the site and extent of MI
o Radioactive dyes
 Thallium (cold spots)
 Technetium 99m (hot spot

Collaborative Management
M- IV Morphine SO4 for pain
O- Oxygen
N- Nitroglycerine
T- Thrombolytics: streptokinase, urokinase, tissue plasminogen
activator
A- Anticoagulants and antiplatelets
R- Rest

Nursing Care
 Position to comfort (semi-fowlers)
 Monitor PR, ECG
 Gradual increase in activity is encourage (sit on chair 1st 24-48hours,
ambulation 4th-5th day)
 Diet-low calories, low cholesterol, low NA, no hot or cold
D. HEART FAILURE
♥ Physiologic state in which the heart cannot pump enough blood to meet the
metabolic needs of the body
♥ Performance of heart depends on FOUR components
o Contractility of the muscle (inotropic state)
o Preload (amount of blood in the ventricle at the end of diastole)
o Afterload (the pressure against which the left ventricle ejects)
o Heart Rate (chronotropic state)
♥ Classified as
o Left-sided failure- failure of side resulting in high oncotic pressures that
push fluid into alveoli of lungs
o Right-sided failure- failure of right side resulting in high oncotic
pressures that push fluid into body tissues

♥ Etiologic includes
o Cardiac causes like MI, hypertension, cardiomyopathies, valve diseases,
fluid overload
o Can occur with normal changes of aging
o Inflammatory diseases
o Congenital defect
o Long-term alcohol abuse
o Chemotoxicity

♥ CHF occurs secondary to the inability of the ventricle to adequately pump


blood
♥ Congestion and backup of fluid can result, leading to pulmonary or systemic
congestion
♥ Consequently, blood flow to avail organs decreases, potentially results in end
organ damage

♥ Manifestations of LSF
 Crackles, SOB, paroxysmal nocturnal dyspnea, dyspnea on exertion,
cough
 Chest pain, orthopnea, wheezing
 Pulmonary edema: frothy/ bloody sputum, cyanosis, pallor,
diaphoresis, severe dyspnea, PCWP> 12 mmHg
 Weakness, nail clubbing, polycythemia
 Cerebral hypoxia, anxiety, syncope
 Lateral displacement of the PMI secondary to ventricular enlargement
and gallops
 Decreased urine output, peripheral vasoconstriction, and hypertention
♥ Manifestations of RSF
 Jugular vein distention, edema
 Easy fatigability, anorexia
 Hepatomegaly, spleenomagaly
 Portal hypertension, ascites
 Jaundice, internal hemorrhoids
 Leg varicositie, weight gain
 Chest pain, S3 and S4 heart sounds
 CVP >10 cm H2O

♥ Management
 Digitalis, diuretic, vasodilator, Oxygen
 Diet (sodium restriction, activity-balanced program)
 Rest, skin care, stool softeners
 Rotating tourniquet

♥ Nursing Management
 Assessing fluid balance
 Auscultate lung sounds
 Determine degree of jugular venous distention
 Identify and evaluate severity of edema
 Monitor PR and BP
 Monitor signs of dehydration
 Assess fluid overload

II. Cardiac Rhythm Disorders


A. Cardiac Dysrhythmia
Sinus rhythm
1. Sinus Node Dysrhytmias
a. Sinus Bradycardia
b. Sinus Tachycardia
c. Sinus Arrhythmia
• Nursing Management:
Assessment: 1. Skin (pale or cool)
2.signs of fluid retention, such as neck vein distention,
and crackles
3. rate and rhythm of apical and peripheral pulses
4. auscultate extra heart sounds (S3 and S4), heart
murmurs, blood
pressure and determine pulse pressure
Diagnosis: 1. Decrease Cardiac Output
2.Anxiety related to fear of the unknown
3. Deficient Knowledge about the dysrythmia and its
treatment
Planning and Goals: ERADICATE OR DECREASING THE INCIDENCE OF
THE DYSRHYTHMIA
Interventions : a. Monitoring and Managing the Dysrythmia
b. Minimizing Anxiety
c. Care for patients with Pacemaker

A. CORONARY ARTERY DISEASE


Definition: abnormal accumulation of lipid, or fatty, substances and fibrous
tissue in the vessel wall which reduces blood flow to the myocardium.

Pathophysiology:
S/S: * chest pain, shortness of breath, unusual fatigue, changes in
ECG, high levels of cardiac enzymes, dysrhythmias, and sudden death.

Medical Management:

B. ANGINA
1. Definition: