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DEFINITION
Heart (or cardiac) failure: pathophysiological state in
which the heart is unable to pump blood at a rate
commensurate with the requirements of the
metabolizing tissues or can do so only from an
elevated filling pressure
According to AHA,
HF is a clinical syndrome including circulatory
congestion or inadequate tissue perfusion , due to
abnormal heart function and associated
neurohormonal abnormalities.
An inadequate or decreased cardiac output which
causes an increase in the blood volume within the
vascular system. The resulting congestion within the
venous system interferes with the movement of body
fluids, resulting in fluid accumulation in the tissue
spaces, causing edema
Frequency : United States
Mortality/Morbidity
Cardiac Physiology
(remember this?)
CO = SV x HR
HR: parasympathetic
and sympathetic tone
SV: preload, afterload,
contractility
Preload
Def: Passive stretch of
muscle prior to contraction
Measurement: Swan-Ganz
LVEDP( venous return)
Really a function of diastole
Affected by compliance
Low compliance = higher LVEDP with lower
LVEDV
Afterload
Def: Force opposing/stretching muscle after
contraction begins
Measurement: SVR
Contractility
5 MAGDI AWAD SASI
Pathophysiology
Hemodynamic changes
Neurohormonal changes
Cellular changes
1.Hemodynamic changes:
HF can be secondary to systolic dysfunction or
diastolic dysfunction
2. Cellular changes
Changes in Ca+2 handling
Changes in adrenergic receptors:
Slight in 1 receptors
1 receptors desensitization followed by down
regulation
Changes in contractile proteins
Program cell death (Apoptosis)
Increase amount of fibrous tissue
3. Neurohormonal changes
Forward Vs Backward
Acute Vs Chronic HF
Low Vs High output HF
Systolic Vs Diastolic HF
A etiology
1. Vascular
Ischemic heart
disease,
myocardial
infarction
2. Valvular
Symptoms:
Left ventricular failureThe patient present with chest symptoms which may delay
the diagnosis and keep the patient to seek chest
consultants advice.
Failure of forward flow from left ventricle into the aorta
result into pulmonary congestion with chest symptoms.
RVF
is caused by:
pulmonale)
3. Cardimyopathies and
myocarditis
SIGNS:
General appearance
Patients with mild heart failure appear to be in
no distress after a few minutes of rest, but they
may be obviously dyspneic during and
immediately after moderate activity. Patients
with LV failure may be dyspneic when lying flat
without elevation of the head for more than a
few minutes. Those with severe heart failure
appear anxious and may exhibit signs of air
hunger in this position.
Patients with recent onset of heart failure are
generally well nourished, but those with chronic
severe heart failure are often malnourished and
sometimes even cachectic.
Chronic marked elevation of systemic venous
pressure may produce exophthalmos and severe
tricuspid regurgitation and may lead to visible
pulsation of the eyes and of the neck veins.
Edema
Bilateral pitting pedal odema.
Usually, a substantial gain of extracellular fluid
volume (ie, a minimum of 5 L in adults) must
occur before peripheral edema is manifested.
Edema, in the absence of dyspnea or other signs
of LV or RV failure, is not solely indicative of
heart failure and can be observed in many other
conditions, including chronic venous
insufficiency, nephrotic syndrome, or other
syndromes of hypoproteinemia or osmotic
imbalance.
16 MAGDI AWAD SASI
Hepatomegaly
Hepatomegaly is prominent in patients with
chronic right-sided heart failure, but it may occur
rapidly in acute heart failure.
When occurring acutely, the liver is usually
tender.
Ascites
This finding occurs in patients with increased
pressure in the hepatic veins and in the veins
draining into the peritoneum.
Precipitating Factors
Infection
Sodium Intake
Medications!!!
Anemia
Thyroid disorders
Endocarditis
Pulm Embolus
Noncompliance
Arrhythmia
Myocardial Infarction
Stress reaction
CBC count
Electrolytes
20 MAGDI AWAD SASI
INVESIVE
1. Exercise stress test
HEART FAILURE 2013
Cardiomegaly
Vascular redistribution
Kerley B lines
Interstitial edema
Peri-bronchial cuffing
Effusions
2. Cardiac
3. Holter monitor
Echocardiogram
Chamber
enlargement
Wall motion
abnormalities
Diminished ejection
fraction
Possible LVH
Possible valvular
problems
Assess diastolic dysfunction
Treatment Goals
Improve symptoms
A. Enhance well-being and quality of life
B. Increase exercise tolerance
Improve survival
A. Prevent progressive heart failure
B. Prevent sudden death
C. Prevent thromboembolic episodes
Treatment ::
26 MAGDI AWAD SASI
Preload Reduction
Loop diuretics Lasix 20-200mg IV (q 6-8 hours)
Nitrates
-Nitroglycerin
IV:10-200 mcg/min
Amrinone / Milrinone n
Digoxin (chronic)
volume overload ,
preload reduction
sodium overload ,
Advantages
Highly effective in most classes
Essential with fluid retention
Well tolerated, simple to use
Disadvantages
Electrolyte abnormalities Na, k ,Ca ,Mg
Hypovolemia, hypotension, renal dysfunction
Activation of neurohormaonal system
AIM----Elimination of symptoms and/or signs of
congestion
Avoid volume depletion
A. Postural hypotension
C. Increase in BUN/Cr
activation
Spironolactone :
Aldosterone inhibition minimize potassium loss, prevent
sodium and water retention, endothelial dysfunction and
myocardial fibrosis.
B-------------ACE Inhibitors
ACE inhibitors should be the initial treatment
for heart failure
Improve hemodynamic status
Attenuate neurohumoral abnormalities
Improve symptoms,
fraction .
Neurohormonal Changes
Decreased angiotensin II.
Reduction in arterial resistance (afterload).
Reduction in venous tension (preload).
Inhibition of cardiac and vascular remodeling .
Increased bradykinin
Decreased or no change in aldosterone
Decreased norepinephrine
Reduction in Sudden Death/Potential Mechanisms
Increase in serum/total body potassium
Decreased adrenergic stimulation
C---------------Beta Blockers
E--------------Vasodilators :
Nursing Responsibilities
Assess heart rate before administration;
if below 60 bpm or above 120 bpm,
withhold the drug.
Monitor serum potassium
Assess for signs of Digitalis toxicity
- Bradycardia
- GI manifestations (anorexia, nausea,
vomiting and diarrhea)
- Dysrrhythmias
- Altered visual perceptions
- In males: gynecomastia, decreased
libido and impotence
Amiodarone and verapamil can increase the plasma
concentration of digoxin by inhibiting its excretion
IN DIASTOLIC FAILURE;
USE B-BLOCKER, ACE-I , CALCIUM CHANNEL BLOCKER
RATE LIMITING
Difficult to treat
Diuretics for volume overload. Avoid volume
depletion
Prevent tachycardia
Rate-limiting calcium channel blockers first choice
Beta 1 beta blockers second choice