NCA DAY 7: HF & CODP (MIDTERM)

HEART FAILURE
● Inability of heart to pump
sufficient blood to meet metabolic
demands of body resulting in
decreased tissue perfusion
● Most heart failure begins with left
ventricular failure and progresses
to failure of both ventricles.
● Compensatory mechanisms
include increased heart rate,
improved stroke volume, arterial
vasoconstriction, sodium and
water retention, and myocardial
hypertrophy.

Left-Sided Heart Failure (Forward

Failure)
● Congestion occurs mainly in the
lungs from blood backing up into
pulmonary veins and capillaries.
- Shortness of breath,
dyspnea on exertion
paroxysmal nocturnal
dyspnea (due to
reabsorption of dependent
edema that has developed
during day), orthopnea,
pulmonary edema
- Cough - may be dry,
unproductive; usually
occurs at night
- Fatigability - from low CO,
nocturia, insomnia,
dyspnea, catabolic effect Right-Sided Heart Failure (Backward
of chronic failure. Failure)
- Insomnia, restlessness. ● Edema of ankles; unexplained
- Tachycardia - S3 weight gain (pitting edema is
ventricular gallop. obvious only after retention of at
least 10 lb [4.5 kg] of fluid)
● Liver congestion - may produce
NCA DAY 7: HF & CODP (MIDTERM)
upper abdominal pain
● Distended jugular veins
● Abnormal fluid in body cavities
(pleural space, abdominal cavity)
● Anorexia and nausea - from
hepatic and visceral
engorgement
● Nocturia - diuresis occurs at night
with rest and improved CO
● Weakness
AW HEAD
● A: Anorexia and nausea
Results from venous
engorgement and venous stasis
within the abd. Organs
● W: Weight gain
Due to retention of fluid
● H: Hepatomegaly
Results from venous
engorgement of the liver;
increased pressure may interfere
with the liver’s ability to function.
● E: Edema (Bipedal)
Edema usually affects the feet
and ankles worsens when the pt.
Stands or sits for a long period.
● A: Ascites
Is the accumulation of fluid in the
peritoneal cavity; increased
pressure within the portal vessels
forces fluid into the abd. cavity
● D: Distended Neck Vein
Increased venous pressure leads
to distended neck veins
Drug Classes
● Diuretics
- To decrease cardiac workload by
reducing circulating volume,
reducing preload- (electrolyte
imbalance?)
- A low-sodium diet and fluid
restriction complement this
therapy.
- Loop diuretics: Give potassium
supplement and potassium rich-
food
- Potassium-sparing
- Thiazides
● Positive inotropic agents -
increase the heart's ability to
pump more effectively by
improving the contractile force of
the muscle.
- Dopamine (Intropin) improves
renal blood flow in low dose
range.
- Dobutamine (Dobutrex).
● Digitalis Glycosides digoxin
(Lanoxin)
- Increases force/strength of
myocardial contraction when
diminished contractility is the
cause of HF, and slows heart rate
by decreasing conduction
through the atrioventricular (AV)
node to decrease the heart rate
and reduces oxygen consumption
- Improved cardiac output
improves renal perfusion,
decreasing renin secretion.
NCA DAY 7: HF & CODP (MIDTERM)
● Monitor serum potassium level
hypokalemia enhances digitalis
toxicity because it potentates the
effect of the drug.
● Report manifestations of digitalis
toxicity: anorexia, nausea,
vomiting, abdominal pain,
weakness, vision changes
(diplopia, blurred vision, yellow-
green or white halos seen around
objects), and new-onset
dysrhythmias.
1 PPT MISSING BEFORE NEXT SLIDE
Management of Heart Failure:
"DAD BOND CLASH"
D: Digitalis
- Increases the force of myocardial
contraction and slows conduction
through the atrioventricular node;
- Improves contractility, increasing
left ventricular output, and
enhances diuresis.
A: ACE Inhibitors
- Promotes vasodilation and
diuresis by decreasing afterload
and preload, ultimately
decreasing the workload of the
heart.
D: Dobutamine
- IV medication administered to
patients with significant left
ventricular dysfunction and
hypoperfusion; stimulates the
beta-1-adrenergic receptors.
B: Beta-blockers
- Reduces mortality and morbidity
in HF by reducing the adverse
effects from constant stimulation
of the sympathetic nervous
system.
O: Oxygen
- Oxygen may be necessary as HF
progresses; need is based on the
degree of pulmonary congestion
and resulting hypoxia.
N: Nitrates
- Causes venous dilation, which
reduces the amount of blood
return to the heart and lowers
preload.
D: Diuretics
- To remove excess extracellular
fluid by
NCA DAY 7: HF & CODP (MIDTERM)
increasing the rate of urine produced in
patients with fluid overload.
C: Calcium Channel Blockers
- Causes vasodilation, reducing
systemic vascular resistance.
L: Lifestyle Changes
- Restriction of dietary sodium,
avoidance of excess fluid intake,
weight reduction, and regular
exercise.
A: Angiotensin II Receptor Blockers
- ARBs block the effects of
angiotensin II at its receptor;
have similar hemodynamic
effects as of ACE inhibitors.
Serves as alternative for patients
who cannot tolerate ACE
inhibitors.
S: Sodium restriction
- A low-sodium diet (2 to 3 g/day)
diet and avoidance of drinking
excess amounts of fluid is
recommended.
H: Hydralazine
- Lowers systemic vascular
resistance and left ventricular
afterload.
Nursing management
Fluid Volume Excess related to
impaired contractility and increased
preload and afterload
● Monitor I and O (especially note
color, specific gravity and
amount) every 2-4 hours and as
needed and 24 hour totals.
- Intake greater than output may
indicate fluid volume excess. If
client receives diuretic therapy,
an increase in output is expected.
● Maintain chair or bed rest in the
semi- fowler's position.
- This position promotes diuresis
by recumbency-induced
increased GFR and reduced ADH
production.
● Weigh daily. Weight loss should
not exceed 1 to 2 lb (0.5 to 1
kg)/day.
- Body weight is a sensitive
indicator of fluid balance.
Daily weights can show
the increase or decrease
in congestion and edema
in response to therapy. A
gain of 5 pounds
represents about 2L of
fluid.
● Assess for jugular neck vein
distention, hepatomegaly,
abdominal pain, edema,
peripheral pulses and presence
of anasarca.
- Elevated volumes in the
vena cava occur from
inadequate emptying of
the right atrium. The
excess fluid is transmitted
to the jugular vein, liver
and abdomen and
manifests as distention.
● Auscultate breath sounds. Note
adventitious sounds, increased
vascular volume and pulmonary
NCA DAY 7: HF & CODP (MIDTERM)
hypertension or worsening of
heart failure.
- These are manifestations of
pulmonary congestion.
● Monitor sudden extreme
shortness of breath and feelings
of panic.
- These are manifestations of
pulmonary edema.
● Note complaints of right uoper
quadrant pain or tenderness.
- Advancing heart failure leads to
venous congestion, which results
in liver engorgement and altered
liver function.
● Evaluate the effectiveness of
diuretics and potassium.
- Fluid shifts and use of diuretics
can alter electrolytes, especially
potassium and chloride
supplements, which affects
cardiac rhythm and contractility.
● Note increased lethargy,
hypotension and muscle
cramping.
- These are manifestations of
hypokalemia and hyponatremia
that may occur because of fluid
shifts and diuretic therapy.
● Elevate legs, avoiding pressure
under knee. Encourage active
and passive exercises. Increase
activity as tolerated. Decreases
venous stasis, and may reduce
incidence of thrombus or
embolus formation.
NOTE: Do not elevate legs if the client is
dyspneic.
● Auscultate heart sounds
frequently and monitor cardiac
rhythm.
> Note presence of S3 - heard during
rapid ventricular filling and failure of the
ventricles to eject blood
> Note presence of S4 - heard during
atrial contractions and often associated
with ventricular hypertrophy
>Monitor for premature ventricular
beats.
● Observe for signs and symptoms
of reduced peripheral tissue
perfusion: cool temperature of
skin, facial pallor, poor capillary
refill of nail beds.
● Monitor clinical response of
patient with respect to relief of
symptoms (lessening dyspnea
and orthopnea, decrease in
crackles, relief of peripheral
edema).
Impaired Gas Exchange related to
alveolar edema due to elevated
ventricular pressures
● Raise head of bed 8 to 10 inches
(20 to 30 cm) - reduces venous
return to heart and lungs;
alleviates pulmonary congestion.
- Support lower arms with pillows - to
eliminate pull of their weight on
shoulder muscles.
NCA DAY 7: HF & CODP (MIDTERM)

- Sit orthopneic patient on side of bed (especially in edematous

with feet supported by a chair, head patients), phlebothrombosis,
and arms resting on an over-the-bed pulmonary embolism.
table, and lumbosacral area supported
with pillows.
● Auscultate lung fields at least
every 4 hours for crackles and
wheezes in dependent lung fields
(fluid accumulates in areas
affected by gravity) and monitor
for frothy sputum production.
- Mark, with ink that does not
easily rub off, the level on the
patient's back where adventitious
breath sounds are heard.
- Use markings for comparative
assessment over time and
among different care providers.
- Observe for increased rate of
respirations (could be indicative
of falling arterial pH)

● Encourage the patient to turn and

cough every 2 hours - to help
prevent atelectasis and
pneumonia.
● Encourage deep-breathing
exercises every 1 to 2 hours - to
avoid atelectasis.
● Offer small, frequent feedings - to
avoid excessive gastric filling and
abdominal distention
● Administer oxygen as directed.
● Administer IV. fluids carefully
through an intermittent access
device to prevent fluid overload.
● Monitor for pitting edema of lower
extremities and sacral area.
● Observe for the complications of
Bed rest - pressure ulcers
NCA DAY 7: HF & CODP (MIDTERM)

parenchyma from
CHRONIC OBSTRUCTIVE injury.
PULMONARY DISEASE - Pollutants or
- Refers to a dse allergens
characterized by airflow - Viral, bacterial, and
limitation that is not fully mycoplasmal
reversible , normally infections.
associated with an CHRONIC BRONCHITIS
inflammatory response of - Defined as the presence of cough
the lungs d/t irritants, w/c and sputum production for at
restricts airflow, damages least 3 months in each of 2
the airways & limits lung consecutive years.
capacity. - Chronic bronchitis is also termed
- CAUSES: as “BLUE BLOATERS”.
- Smoking: - Irritation of airways results in
Depresses the inflammation and hypersecretion
activity of of mucus —> Mucus-secreting
scavenger cells and glands and goblet cells increase
affects the in number —> Ciliary function is
respiratory tract’s reduced, bronchial walls thicken,
ciliary cleansing bronchial airways narrow, and
mechanism. mucus may plug airways —>
- Occupational Alveoli become damaged and
exposure: fibrose, and alveolar macrophage
Prolonged & function diminishes —> the pt is
intense exposure to more susceptible to respiratory
occupational dust & infections
chemicals, indoor
- air pollution, and
outdoor air
pollution.
- Genetic
Abnormalities:
deficiency of
alpha1-antitrypsin
(synthesized by the
liver), an enzyme
inhibitor that
protects the lung
NCA DAY 7: HF & CODP (MIDTERM)

- (Cont.) alveolar hypoxia —> - Hemoptysis

Pulmonary vasoconstriction —> - Mild dyspnea
pulmonary hypertension —> RHF initially
(Cor Pulmonale) - Cyanosis (d/t
hypoxemia)
- Peripheral edema
(d/t cor pulmonale)
- Crackles, wheezes
- Prolonged
expiration
- Obese
- Complications:
- Secondary
polycythemia vera
d/t hypoxemia
- Pulmonary
hypertension d/t
reactive
vasoconstriction
from hypoxemia
- Cor pulmonale from
chronic pulmonary
hypertension

EMPHYSEMA
- A pathological term that
describes an abnormal distention
of the air spaces beyond the
terminal bronchioles, w/
destruction of the walls of the
alveoli.
- “PINK PUFFER” - EMPHYSEMA
- Symptoms:
- Dyspnea
- “BLUE BLOATER” - CHRONIC - Minimal cough
BRONCHITIS - Increased minute
- Symptoms: ventilation
- Chronic, productive - Pink skin, pursed-lip
cough breathing
- Purulent sputum
NCA DAY 7: HF & CODP (MIDTERM)

- Accessory muscle
use
- Cachexia
- Hyperinflation,
barrel chest
- Decreased breath
sounds
- Tachypnea
- Complications:
- Pneumothorax d/t
bullae
- Wt loss d/t work of
breathing
- Pathophysiology
- Alpha1-antitrypsin
deficiency —> increase
neutrophil elastase —>
unopposed breakdown of
elastin fib