CONGESTIVE HEART FAILURE

• A general term to describe several types of cardiac dysfunction that result in inadequate perfusion
of tissues with vital blood—borne nutrients.

• The systemic response in decrease CO.

• The hearts response in increase blood volume.

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

CLASSIFICATION OF HEART FAILURE:

DESCRIPTION
CLASS I No symptoms noted with normal activity
CLASS II Symptoms noted with normal activity but subside with rest
CLASS III Symptoms noted with minimal activity; may or may not be symptom free at rest
CLASS IV Symptoms usually present at rest and worsened at any type of activity

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.

LEFT SIDED HEART FAILURE

• 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

• Common cause- is MYOCARDIAL INFARCTION

PATHOPHYSIOLOGY

Backward Effects
 ↑ volume and end- diastolic
Emptying of LV pressure in LV ↑ volume in LA

Raoid filling of Transudation of fluid from

alveolar spaces capillaries to interstitial ↑ volume in capillary
spaces of alveoli bed

Fluid in alveoli Bronchoconstriction Pulmonary edema

S/S: wheezing (cardiac asthma)

S/S: dyspnea, dec. O2 sat.,

DEATH shock increased RR, orthopnea,
PND

FORWARD EFFECTS

Perfusion of tissues BLOOD flow to kidneys

Cardiac output
of the body and glands

s/s:Pulsus s/s: easy fatigability,

alternans Weakness, dizziness

Secretion of Na & Reabsorption of Na & H2O

H20-retaining hormones Vasoconstriction

Total blood vol &

ECF volume
Increased systemic BP

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

RIGHT SIDED HEART FAILURE

• Impairs the ability to move deoxygenated blood from the systemic circulation into the pulmonary
circulation

• Blood goes back to the systemic 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)

Decrease systemic blood flow & pressure

Increases pressure in the
great veins and distensible
organs
= dec. tissue perfusion to organs such as the
kidneys
SNS stimulation , Inc. blood volume & vasoconstriction

Inc. Jugular vein distention

pressure in
capillary
vessel
=
dependen Hepatomegaly ,
t Spleenomegaly
peripheral
edema
Inc. pressure in peritoneal
vessels
= ascites

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

VENTRICULAR ASSIST DEVICE

• Is a mechanical circulatory device that is used to partially or completely replace the function of the
failing heart.
• HEART TRANSPLANTATION
• CARDIOMYOPPLASTY
 INFECTIOUS HEART DISEASE

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

ETIOLOGY & RISK FACTORS

Risk factors
1.Most often bacterial but may be fungal or viral.

2.History of preexisting heart condition.

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

Nonbacterial Thrombotic Endocarditis

Genitourinary Hemodialysis
instrumentation

Dental procedure IV drug abuse

Skin Infection Cardiac Surgery

BACTEREMIA

Local valve damage

Infiltration of supporting structures

Sepsis Heart Failure Heart Block

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

E NSURE BED REST

N SAID
D OPPLER SCAN
O BSERVE EMBOLIZATION
C ULTURE OF BLOOD
A NTIBIOTIC REGIMEN
R HD PRECAUTION
D RUG FOR FEVER AND JOINT PAIN
I NTAKE AND OUTPUT MONITORING
U PHOLD GOOD ORAL HYGIENE
M ANAGE VALVULAR DEFECTS