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 from left
valves ventricle to left atrium (mitral valve)
 Semilunar valves Prevent backflow from pulmonary artery to right 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 the left
artery ventricle and posterior septal wall, SA node , AV node
 Left Coronary
Artery:
- Left anterior Supplies blood to anterior wall of left ventricle, anterior ventricular
descending septum, and apex of the left ventricle
artery
- Circumflex Provides blood to left atrium, lateral and posterior surfaces of the left
artery 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 synchronous
branches, Purkinje’s fiber contraction of ventricles

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 1 st 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: