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• A general term to describe several types of cardiac dysfunction that result in inadequate perfusion
of tissues with vital blood—borne nutrients.
Risk factors:
MNEMONICS:
R- enal disease
A- nemia
P- ulmonary embolism
I- nfection (myocarditis, Pericarditis)
D- elivery after pregnancy
F- orget to take the meds
A- rrhythmias
I- ischemia/infarction
L- ipid aggregation
U- ncontrolled hypertension
R- HD
E- ndocarditis
COMPENSATORY MECHANISM – heart failure commences when an event or condition such as MI,
hypertension or diabetes causes a decline in the heart’s pumping capacity, leading to the activation of
compensatory mechanism. The rennin-angiotensin-aldosterone system kicks in to attempt to restore cardiac
function. Overtime, however, end-organ damage occurs, leading to left ventricular remodeling.
• Occurs when left side of the heart is unable to pump the total volume of blood it receives from the
right side of the heart
PATHOPHYSIOLOGY
Backward Effects
↑ volume and end- diastolic
Emptying of LV pressure in LV ↑ volume in LA
FORWARD EFFECTS
s/s: S3 gallop
CLINICAL MANIFESTATIONS
• Dyspnea in the early stages
• Decreases O2 saturation
• Increase RR
• Easy fatigability, weakness and dizziness
• Orthopnea
• Auscultation reveals S3 gallop
• Pulsus alternans
• Paroxysmal Nocturnal Dyspnea
• Cardiac asthma
• Acute pulmonary edema= life-threatening since it may progress to shock & death
• Impairs the ability to move deoxygenated blood from the systemic circulation into the pulmonary
circulation
• Systemic circulation is congested (backward effect); output to lungs is decrease (forward effect)
Etiology
• Persistent left sided heart failure
• Stenosis / Regurgitation of tricuspid or pulmonic valves
• Right ventricular infarction
• Acute / chronic pulmonary disease: COPD, severe pneumonia, pulmonary embolus
• Pulmonary hypertension (cor pulmonale)
CLINICAL MANIFESTATIONS
• Major manifestation: PERIPHERAL EDEMA
• Weight gain
• Hepatomegaly
• RUQ pain
• Splenomegaly
• Ascites
• Anorexia and abdominal discomfort
• JV distention
DIAGNOSTIC TESTS
• Chest x-ray
• Echocardiography
• Elevated SGPT
• Decrease CVP
NURSING DIAGNOSES
1. Decreased cardiac output
2. Fluid Volume Excess
3. Impaired Gas Exchange
4. Ineffective Tissue Perfusion
5. Risk for Activity Intolerance
6. Risk for impaired skin integrity
7. Risk for Anxiety
PATHOPHYSIOLOGY
Weakened heart muscle, restrict
blood flow to the LUNGS
(Increase pulmonary pressure)
Goals:
1. To monitor for reduced cardiac workload
2. To maintain adequate fluid balance
3. To reduce myocardial workload
4. To monitor for pulmonary edema
5. To assess response to medical therapies
INTERVENTIONS
U- pright position
N- itrates
L- asix, dieuretics
O- xygen
A- minophylline
D- igoxin
F- luids decrease
A- fterload decrease (ace, beta, ca)
S- Na restriction
T-est (monitor diff electrolytes), SFF
SURGICAL MANAGEMENT
ENDOCARDITIS
- inflammation of the endocardium
- bacterial/nonbacterial
INEFFECTIVE ENDICARDITIS
• a relatively uncommon, life-threatening infection of the endocardial surface of the heart, including
the heart valves.
• FORMS:
– Subacute Bacterial Endocarditis (SBE)
– Acute Bacterial Endocarditis (ABE)
– Native Valve endocarditis
– Prosthetic valve endocarditis
– Nonbacterial thrombotic endocarditis
Risk factors
1.Most often bacterial but may be fungal or viral.
3.History of recent invasive procedures: minor surgery, dental procedures, procedures involving the urinary
tract.
Etiology:
- S. Aureus
- Streptococci
- HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, kingella)
Turbulent blood flow
High (valvular dysfunctionn)
Cold Altitude
Exposure
Stress
SLE,
RHD
Cardiac
Catheterization
Endothelial damage
Development of Thrombi
Genitourinary Hemodialysis
instrumentation
BACTEREMIA
Clinical Features:
– Osler’s Nodes
– Janeway’s Lesions
– Petecchiae
– Splinter hemorrhage (fingernail)
– Murmurs
Diagnostics:
1. History to identify site of entry.
2. Echocardiography
3. Blood cultures
4. CBC
5. ESR
6. DUKE Criteria
DUKE’S CRITERIA
MAJOR CRITERIA
1. Positive Blood Culture
2. Evidence of endocardial involvment (+ echocardiogram)
MINOR CRITERIA
1. Predisposition: Predisposing heart condition or injection drug use
2. Fever > 38 degrees Celsius
3. Vascular phenomena: Janeway lesions, conjunctival hemorrhage, intracranial hemorrhage, major
arterial emboli, septic pumonary infarcts,
4. Immunologic phenomena: glomerulonephritis, Osler’s node, Roth’s spots, Rheumatoid factor,
5. Microbiologic evidence: positive blood culture not meeting major criterion
NURSING DIAGNOSES
1. Hyperthermia
2. Decreased Cardiac Output
3. Activity Intolerance
4. Deficient Knowledge
GOALS:
1. Attainment of normal or baseline cardiac function
2. Performance of ADL without fatigue
3. Knowledge of therapeutic regimen
Treatment:
A. IV antibiotic therapy for 4 to 6 weeks
B. Bed rest if high fever or evidence of cardiac damage is present
C. Prophylactic antibiotics for 3 to 5 years, especially in children with history of rheumatic fever or
congenital anomalies.
D. Surgical interventions for severe valvular damage.
NURSING RESPONSIBILITY