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Transcript
Nursing and heart failure
Congestive Heart Failure (CHF) or cardiac
failure, is one of the most common causes
of in-hospital mortality for patients with
cardiac diseases. It is the second most
common complication after myocardial
infarction (MI). Men are affected more than
women. The 5 year mortality rate for men
is 60% and about 45% for women.
The aim for nurses
- to improve patient outcomes and quality of
patient’s life
- to decrease hospital admissions and,
therefore, cost
Definition
Congestive Heart Failure indicates the
inability of the heart to pump enough blood
to meet the body’s metabolic requirements
for oxygen and nutrients leading to
discrepancies between myocardial oxygen
supply and demand.
PATHOPHYSIOLOGY
Changes in:
-
heart rate
stroke volume
contractility
preload
afterload
Compensatory Mechanisms
- ADRENERGIC MECHANISM
- RENAL MECHANISM (RENIN-ANGIOTENSINALDOSTERON SYSTEM)
- VENTRICULAR HYPERTROPHY
ETIOLOGY
-
coronary heart disease
long-standing hypertension
cardiomyopathy
valvular dysfunction, valvular diseases
inflammatory or degenerative cardiac
muscle diseases
Precipitating factors
-
cessation of cardiac drug intake
dysrythmias
fever
hypoxia
hypoxemia
anemia
respiratory and/or metabolic acidosis
electrolyte imbalance
CLASSIFICATION
-
-
-
Right-Sided Cardiac Failure
Left-Sided Cardiac Failure
Forward Cardiac Failure (inability of the right and left ventricles to pump
blood into the pulmonary and systemic circulation, respectively. It occurs
due to increased pressure in the arterial system (afterload) causing
decreased cardiac output and hypoperfusion of vital organs. This frequently
occurs with aortic stenosis and/or systemic hypertension)
Backward Cardiac Failure (inadequacy of the ventricles to empty the blood
into the arterial circulation. This causes accumulation of fluid and elevation
of pressure (e.g. increasing in all chambers of the heart and in the venous
system behind the affected ventricles). Myocardial infarct and
cardiomyopathy causes decreased systolic ejection which can lead to
backward CHF)
Acute and Chronic Cardiac Failure
Low ventricular output (infarction, hypotension, cardiomyopathy or
hemorrhage) and high ventricular output (fever, thyrotoxicosis, anemia,
pregnancy) CHF
Assessment Parameters
- Respiratory Assessment
- Cardiovascular Assessment (including
capillary wedge pressure)
- Renal Function Assessment
- Peripheral Assessment
- CNS Assessment
Laboratory Result Analysis
- arterial blood gases
- liver function tests
- kidneys function tests
Pharmacological Management
- Increasing Oxygen Supply
- Decreasing Oxygen Demand (Positive
Inotropic Agents) – cardiac glycosides
- Negative chronotropic agents (betablockers, calcium channel blockers)
- Reducing afterload and preload
(nitrates, hydralazine, angiotensinconverting enzyme (ACE) inhibitors)
- Diuretics (Thiazides, Loop Diuretics)
Nursing Interventions
- Promoting Rest
- Promotion of Tissue Perfusion (moderate
daily exercise, adequate oxygen administration as ordered, and
diuresis)
- Fluid and Dietary Considerations
Patient Education
Patient teaching is one of the most important factors in nursing
management of congestive heart failure. Recurrent episodes of
cardiac failure are often due in part to noncompliance, such as
failing to follow medication therapy, straying from dietary guidelines,
missing medical appointments, engagement in excessive and
unregulated exercise, and failing to recognize recurring symptoms.
Topics which should be covered in teaching include: gradual
increase in activity as tolerated, which should be discontinued when
symptomatic; medication actions, side effects, dosage, scheduling,
administration, and signs of toxicity; encouragement of medical
follow ups; report of any untoward symptoms that could indicate
worsening of the condition (shortness of breath, nocturnal dyspnea,
productive cough, ankle edema, anginal pain, palpitations, and
extreme fatigue); maintaining weight; sodium and fluid restriction;
prevention of infection, and avoidance of coffee and tobacco, which
increase the workload on the heart by increasing sympathetic
stimulation and causing vasoconstriction.