INFECTIOUS HEART DISEASES

• rhd
• ENDOCARDITIS
• PERICARDITIS

RHEUMATIC HEART DISEASE (rhd)

 Develops after an episode of group A beta hemolytic streptococcal pharyngitis
 Initially as rheumatic fever then develops into rheumatic heart disease
 Characterized by a new heart murmur, cardiomegaly, pericarditis and heart failure
 Prompt antibiotic treatment can prevent its development
 Other causative factors are due to malnutrition, overcrowding, and lower
socioeconomic status

PATHOPHYSIOLOGY
 Injury is caused by an inflammatory or sensitivity reaction to streptococci
 Leucocytes accumulate in the affected tissues and form nodules, which eventually
are replaced by scar tissue
 Myocardium is involved, weakening the contractile power of the heart
 Could also involve the pericardium
 Anatomic finding of a tiny translucent vegetations or growth, resembling the size of
pinhead, in the valve leaflet
 The flaps gradually become shorter and thicker which prevents them from closing
the orifice completely
 Results in valvular regurgitation (leakage), most common is MR (mitral regurgitation)
 Complications include intractable heart failure and serious dysrhythmia

Streptococcus infection
Bacterial proliferation releasing M-protein
Ag-Ab complex
Treated with inflammatory immune response

Another streptococcal infection

↑↑ Ab production against Ag (M-protein)
Autoimmune response
Chronic valvular disease

CLINICAL MANIFESTATIONS
 “Heart murmurs” due to valvular stenosis, regurgitation is heard on auscultation
 “thrills” on palpation
 Cardiac symptoms depend on which side of the heart is involved, severity depends
on the size and location
 Mitral valve is most often affected, producing symptoms of left-sided heart failure like
shortness of breath, crackles and wheezes
 Throat culture is necessary for diagnosis
 If culture is positive, give prescribed antibiotics
 Penicillin is the drug of choice
 Instruct patient to complete the dose of antibiotics to prevent complication to RHD
  Signs and symptoms:
1. Rheumatic Fever (38.9 -40 ºC)
History of sore throat
h/a
abdominal pain
lympadenopathy
acute sinusitis
↑↑ ESR,
Fever spikes in the late afternoon
2. Carditis
Mitral and aortic valve --- fibrous scar tissue --- valve deformity
Edema: face, abdomen, ankle
3. Migratory polyarthritis
Most common finding
Involves major joints (knees, elbows, wrists)
Responds to ASA
4. Erythema marginatum
Most commonly seen on trunk and inner aspects of upper arm and thigh
Linear rashes
5. Subcutaneous nodules
Hard, painless, freely movable
6. Sydenham’s chorea
Spontaneous, rapid, purposeless, jerking movements
Patients are fidgety, cries easily, begins to walk clumsily, drops things

Major symptoms Minor symptoms

Carditis history of rheumatic fever
Polyarthritis recent history of strep infection
Chorea increased ESR and ASO titer
Subcutaneous nodule
Erythema marginatum
JONES CRITERIA:
2 major criteria
1 major + 2 minors

MEDICAL MANAGEMENT
 Prophylactic IM dose of penicillin every 3-4wks for 5 yrs or until age 21 yrs old
 Erythromycin is the drug of choice for patients allergic to penicillins
 ASA and corticosteroids as supportive managements
 For patients who has undergone invasive procedure, Erythromycin, Azithromycin
and Clarithromycin as alternatives for Penicillin allergy

NURSING MANAGEMENT
 Warn patients on the occurrence of streptococcal pharyngitis
 Key nursing role is teaching patients about the disease, its treatment, and the steps
needed to avoid complications
 Educate patient and community regarding recognition of streptococcal infections and
need for adequate treatment
 Carditis:
Administer Pen as ordered
 Promote bed rest until ESR returns to normal (limit activities)
 Arthritis
Aspirin as ordered
Change position frequently
Cutaneous stimulation and alt. hot and cold application
 Chorea
Decrease stimulation
Initiate seizure precautions

INFECTIVE ENDOCARDITIS
 microbial infection of the endothelial surface of the heart
 usually develops in people with prosthetic heart valves, structural defects (valve
disorders), older individuals, low immunity
 Etiologic agents: streptococci, staph, entero or pneumococci
 Vegetations may embolize to other tissues throughout the body
 Acute Bacterial Endocarditis (ABE)-rapid onset of infection, days to weeks
Staphylococcus aureus (common in IV drug users)
 Subacute Bacterial Endocarditis – 2 weeks to months
Streptococcus viridans

 Systemic emboli occur in left-sided infection

 Pulmonary emboli occur with right-sided infection

PATHOPHYSIOLOGY:
Infective organism enter the blood stream
Travel and reach the hear valves and endocardium
Deposition in the endocardium producing inflammation
Inflammatory process:
Fibrin formation
Platelet aggregation
deposition of vegetation on heart valves
ulceration and valvular necrosis
deformity and valvular dysfunction

CLINICAL MANIFESTATIONS
 Insidious onset, s/s develop from the toxic effect of the infection
 Presenting symptoms are fever and heart murmur
 Fever may be intermittent or absent, esp in those taking antibiotics or
corticosteroids
 Murmurs that worsen indicate progressive damage from vegetations of the valve
 Oslers nodes- small painful nodules in the pads of fingers or toes
 Janeway lesion- painless, red flat macules on the palms and soles
  Roth spots – hemorrhages with pale centers caused by emboli in the nerve fiber
layer of the eye
 Splinter hemorrhages – reddish brown lines and streaks under fingernails and
toenails
 May have cardiomegaly, heart failure, tachycardia and splenomegaly

MEDICAL MANAGEMENT
 Prophylactic antibiotic given to high risk patients
 2 gms of Amoxicillin given 1 hour before dental, oral, respiratory or esophageal
procedures
 Antibiotic therapy given IV for 2-6 weeks
 Pen G is the drug of choice
 Blood cultures taken periodically
 Fungal endocarditis – Amphotericin B

NURSING MANAGEMENT
 Administer antibiotics as ordered.
 Control temperature elevation by antipyretics
 Assess heart sounds – progressive murmur may indicate worsening
 Monitor s/s of systemic embolization, pulmonary or nervous system involvement
(vascular involvement)
 Emphasize the need for prophylactic antibiotics
 Provide client teaching:
 Types and procedures that increase the chances of recurrences may need
prophylactic antibiotics

PERICARDITIS

 Inflammation and infection of the visceral and parietal pericardium

 due to bacterial, viral or fungal infection; trauma, acute MI, neoplasms,
uremia

CLINICAL MANIFESTATIONS
 Sharp, sudden chest pain over the precordium, radiation to the neck and
left scapula, aggravated with deep inspiration or movement and relieved
by sitting up and leaning forward
 Pericardial friction rub precipitated by coughing and twisting of trunk
 Hemoptysis, malaise, orthopnea
 Tachycardia, fever and cyanosis or pallor
 Distant heart sounds
 JVD due to accumulation of fluid
DIAGNOSTIC TEST
 Elevated WBC and ESR
 CXR may show increased heart size
 ECG changes (T wave inversion and diminished QRS complex)
 Pericardiocentesis reveals positive pericardial fluid culture

NURSING INTERVENTION
 Corticosteroid, Morphine, Salicylates to reduce inflammation and provide pain relief
 Specific antibiotic therapy against identified causative organism
 Ensure comfort: bed rest with semi/high fowlers
 Client teaching and discharge planning concerning:
o s/sx of pericardiits indicative of a recurrence (chest pain intensified by
inspiration and position changes, fever, cough)
o medication regimen including name, purpose, dosage frequency, s/e)

cardiomyopathy

• subacute or chronic disorder of the heart muscle

• treatment is palliative

1. Dilated Cardiomyopahty
Most common type
Hx of specific exposure to etiol. agents (ROH, Metamphetamine)
Condition: heart ejects less than 40% of blood in the ventricles
↓↓
↓↓ cardiac output
↓↓
Heart failure

Assessment
Symptoms of left ventricular heart failure
Weakness and fatigue
Activity intolerance
Chest pain
Eventually signs of right sided heart failure

Implementation
Symptomatic treatment of heart failure
Diuretics, cardiac glycosides and vasodilators ( ↑↑ CO)
Remove/avoid offending agents

2. Hypertrophic Cardiomyopahty

Massive ventricular hypertrophy which causes:

Reduction of ventricular cavities
Decrease ventricular filling during diastole
Increased septal size (causing the mitral valve and septum to obstruct outflow)
 Assessment
Exertional dyspnea
Syncope
Chest pain that occurs at rest and is not relieved by nitrates
Dysrythmias

Implementation
Symptomatic treatment
Cardioversion (atrial fibrillation)
Avoid alcohol
Report dizziness or fainting (indicates dysrhythmias)
Administer Ca channel blockers and beta blockers
Vasodilators and cardiac glycosides are contraindicated
Cardiac muscle resection with mitral valve replacement (ventriculomyotomy)

3. Restrictive Cardiomyopathy
Restriction of filling of the ventricles due to rigid walls causing:
Severe diastolic noncompliance of both ventricles
Increase in LV/RV filling pressure
Pulmonary congestion
Right sided heart failure

CARDIAC TAMPONADE
Accumulation of fluid in the pericardial sac compressing the heart
May follow pericarditis, advanced heart failure, metastatic Ca, trauma, surgery

PATHOPHYSIOLOGY:
Increased fluid production
↓↓
Increased intra-pericardial pressure
↓↓
Decreased venous return
↓↓
Decreased ventricular filling
↓↓
Decreased CO

CLINICAL MANIFESTATIONS
BECK’S TRIAD: narrowing pulse pressure
rising venous pressure ---engorged neck veins
distant muffled sound
↓↓ BP and pulsus paradoxus

MEDICAL MANAGEMENT
Pericardiocentesis – aspiration of fluid in the pericardial sac
Pericardiotomy – excision of a portion of the pericardium

Valvular heart disease

Stenosis – heart valves cannot fully open
Regurgitation (insufficiency) – heart valves cannot close completely

Types:
1. Mitral Valve Prolapse: valve leaflets protrude into the LA during systole
2. Mitral Stenosis : valvular tissue thickens and narrows the valve opening
3. Mitral Insufficiency: incomplete valve prevents complete closure
4. Aortic Stenosis / Aortic Insufficiency
6. Tricuspid Stenosis / Tricuspid Insufficiency
9. Pulmonary Stenosis / Pulmonary Insufficiency

DIAGNOSTIC PROCEDURE: ECHOCARDIOGRAPHY

SURGICAL REPAIR PROCEDURES

A. Valvuloplasty – repair of cardiac valves
1. Commisurotomy
a. Closed Commisurotomy
• Balloon Valvuloplsaty: balloon inflated to enlarge the orifice
b. Open Commisurotomy (open heart surgery)
• Valves are visualized – thrombi removed – fused leaflets
are incised – calcium deposits are debrided from the leaflet

2. Annuloplasty – tightening and suturing the malfunctioning valve annulus

B. Valve Replacement
1. Mechanical Prosthetic Valves
Very durable but can fail
Thromboembolism may occur
Lifetime anticoagulant therapy is required
2. Bioprosthetic Valves
Little or no clot formation

MITRAL VALVE PROLAPSE

• Mitral valve leaflet balloons back into the left atrium
during systole
• Incidence: ♂ < ♀
• ASSESSMENT:
Fatigue
Atypical chest pain
Palpitation and tachycardia
Dizziness and syncope
Systolic click (earliest sign)

MITRAL INSUFFICIENCY/REGURGITATION
• Blood flowing back from the left ventricle
• ASSESSMENT:
CHF symptoms: dyspnea, fatigue, weakness, JVD, edema
High pitched systolic murmur
MITRAL VALVE STENOSIS
• Obstruction of blood flowing from the LA to the LV
• Most often caused by rheumatic endocarditis
• Leaflets fuse together causing obstruction
• ASSESSMENT:
Dyspnea, orthopnea
Symptoms of RSCHF
Rumbling apical diastolic murmur
AORTIC STENOSIS
• Congenital or acquired after rheumatic endocarditis
• Increases pressure on the left ventricle
• ASSESSMENT:
Exertional dyspnea
Angina
Dizziness and syncope
Harsh systolic crescendo-decrescendo murmur

AORTIC INSUFFICIENCY
• Flow of blood back to the LV from the aorta during diastole
• Due to: endocarditis, syphilis, dissecting aortic aneurysm
• ASSESSMENT:
Dyspnea, orthpnea
Angina, fatigue
Blowing crescendo diastolic murmur (strong/forceful heart sound)
Widened pulse pressure

INTERVENTIONs:
~eliminate caffeine and ROH from the diet
~administer medications as prescribed
β-blocker for chest pain and palpitations
Ca-channel blocker
~administer prophylactic antibiotics when necessary
~administer treatment for heart failure:
O2 inhalation
Digoxin and diuretics
Low sodium diet
~prepare for surgical procedures

Dysrhythmias
• Disorders of the formation and/or conduction of the electrical impulse within
the heart
• Cause disturbance in heart rate and rhythm of the heart
• Diagnosed by analyzing the ECG
• Named according to the site or origin of the impulse and the mechanism of
formation or conduction involved
• Site of origin • Mechanism of formation or
conduction
o Sino-atrial (SA) node o Normal rhythm
o Atria o Bracycardia
o Atrio-ventricular (AV) node or o Tachycardia
junction o Dysrhythmia
o Flutter
o Fibrillation
o Premature complexes
o Blocks
A. Sinus Node Dysrhythmias
• Impulse is created by the sinus
• P to QRS ratio is 1:1
• Treatment directed at the cause and done symptomatically

1. Sinus Bradycardia: slower than normal propagation

Ventricular and atrial rates below 60
Causes Treatment

Lower metabolic needs (hypothermia, Atropine sulfate

hypothyroidism) O2 administration
Vagal stimulation (vomiting, suctioning, extreme Pacemaker insertion
emotions)
Medications (Ca channel blocker, β blocker)
Increased intracranial pressure
MI

2. Sinus Tachycardia: faster than normal propagation

Ventricular and atrial rates above 100
Causes Treatment

Acute blood loss Ca channel blocker

Hypervolemia/hypovolemia β blocker
CHF
Pain
Hypermetabolic states (fever, exercise, anxiety)
Sympathomimetic medications

3. Sinus Arrhythmia: irregular rhythm

Rate increases with inspiration and decreased with
expiration
No hemodynamic changes
No Treatment necessary

B. Atrial Dysrhythmias
1. Premature Atrial Complex:
• single ECG complex that starts in the atrium before the next normal impulse
from the SA node
• P:QRS ratio is 1:1
Causes Treatment

Caffeine, alcohol, nicotine <6/mm - no treatment

Stretched atrial myocardium >6/mm - tX directed at cause
(hypervolemia)
Hypermetabolic state
Atral ischemia, injury or infarction

2. Atrial Flutter (Saw-toothed ECG)

• Not all impulses from the atria is conducted to the ventricle
• P:QRS ratio is 2-4:1
Associated with: Treatment:

Valvular heart diseases  to slow conduction of AV:

CAD Diltiazem
HPN β – blocker
Cardiomyopathy Digitalis
Hyperthyroidism
Pulmonary disease  to restore normal rhythm
Aftermath of open heart surgery Cardioversion/ countershock
(synchronized with the R wave of the
Clinical manifestation: ECG)
Chest pain
SOB
hypotension

3. Atrial Fibrillation (atrial rate 350-600bpm)

• disorganized impulses from the atria
• Atria may quiver resulting in thrombi formation
• P wave absent (P:QRS ratio not discernible)
Clinical Manifestation: Treatment:

Palpitation  To achieve conversion to sinus

Fatigue rhythm
Malaise Quinidine
Pulse deficit (apical ≠ Amiodarone
peripheral) Digoxin
Verapamil

C. Ventricular Dysrhythmias
1. Premature Ventricular Contractions (“Skip Beat”; “Quadrigeminy”)
• Impulse starts at the ventricle and conducted before the next normal sinus
impulse
• Causes:
o In healthy people: intake of caffeine, nicotine or smoke
o Cardiac ischemia or infarction
o Increased workload of the heart
o Digitalis toxicity
o Electrolyte imbalance

• In the absence of disease, PVCs are not serious

• In clients with MI, PVCs suggests more aggressive therapy
• Treatment: Lidocaine!!!!!!!!!!!!!!!!!!!

2. Ventricular Tachycardia
• Similar causes with PVCs
• Stable clients with sustained VT – O2 and antidysrhythmic drugs
• Unstable patients: + cardioversion, CPR
• Pulseless VT: defibrillation and CPR!!!!!!!!!!!!!!!!!!!!!!!!

3. Ventricular Fibrillation
• Rapid but disorganized ventricular rhythm
• No atrial activity
• Absence of audible heart beat and respirations and palpable pulse
• Treatment: defibrillation!!!!!!!!!!!!!!!!
• Rapidly fatal if not terminated within 3-5 minutes

4. Idioventricular Rhythm/ ventricular escape rhythm

• Occurs when the impulse starts in the conduction system below the AV node
• Commonly causes the patient to lose consciousness and other ssx of
reduced CO
• Treatment: IV Atropine as ordered !!!!!!!!!!!!!!!

5. Ventricular Asystole
• “Flat line without treatment”
• Emergency measure: CPR

D. conduction Abnormalities
• Causes: medication
MI or ischemia
Valvular disorders
Myocarditis
• Types
1. first degree AV block: rarely causes hemodynamic change
  Conduction of impulse in the SA node is delayed
 PR interval is more than 0.2seconds

2. Seconds degree AV block

Type I – atrial impulse takes longer time for conduction than the one
before it, until
one impulse is fully blocked
Type II – only some of the atrial impulses is conducted

3. Third Degree AV block/ Complete heart block

 No atrial impulse is conducted to the ventricles
 Two impulses stimulates the ventricles

• Clinical manifestation: SOB, chest pain, lightheadedness, ECG

changes
• Treatment directed at increasing the HR to maintain normal CO
• No treatment is indicated for stable, asymptomatic patient
• Treatment options: Atropine Sulfate, Pacemaker implantation!!!!!!!!!
MANAGEMENT OF DYSRHYTHMIAS
1. Vagal stimulation to terminate supraventricular tachydysrhythmias
o Carotid massage
o Valsalva maneuver

2. cardioversion
• Synchronized counter-shock to convert an undesirable rhythm to stable
rhythm

3. defibrillation (emergency treatment)

• Asynchronous counter-shock used to terminate pulseless VT or VF
• Three rapid consecutive shocks: 200 joules, 300 joules and 360 joules

4. Automatic external defibrillator (AED)

5. Implantable Cardioverter Defibrillator (ICD)
• Stable patients – at risk of VTach/ Vfib

6. Anti-arrhythmic Medication
~Class I – Na+ channel blocker
Quinidine, Procainamide, Dipyridamole!!!!!
Lidocaine (short term emergency med)!!!!!
~Class II – Beta blockers
~Class III – K+ channel blockers: Amiodarone IV!!!!!
~Class IV – Ca+ channel blockers

7. Pacemakers:
• Devices that provide electrical stimulation to the heart to maintain the
heart rate when the client’s pacemaker fails
• Settings:
1. synchronous or demand pacemaker (heart cannot conduct
electrical stimuli)
 2. asynchronous or fixed rate – specific rate
3. overdrive pacing – dos/initiate all electrical impulses

• Types:
1. temporary pacemakers
2. permanent pacemakers

NURSING INTERVENTIONS
1. monitoring and managing the dysrhythmias
Evaluate pulse rate
Respiratory rate and depth
Breath sounds

assess for episodes of lightheadedness, dizziness or faintness

2. obtain 12L ECG

3. Administer antidysrhythmic drugs as prescribed
4. assess contributing factors to dysrhythmias
5. Supportive management: O2 inhalation
6. minimize anxiety