HEART FAILURE
Hypertension
● the heart's ability to effectively pump blood
is compromised
● leads to inadequate oxygen/nutrient supply
to the body's tissues.
● left side of the heart: its higher workload and
pressure load.
● Key factors contributing to left-sided heart
failure includes:
○ the heart's role in systemic
circulation
○ Overall, the heart's role in systemic
circulation is to continuously pump
oxygenated blood from the left side
to all parts of the body, ensuring the
supply of nutrients and oxygen and
facilitating the removal of waste
products.
Causes
1. Coronary Artery disease
a. Cholesterol and fat deposits
accumulate in heart arteries.
b. Reduced blood and oxygen flow to
heart muscle.
c. Heart works harder, potential muscle
damage.
2. Heart attack:
a. Blocked artery to heart.
b. Lack of oxygen damages muscle, it
dies.
c. Rest of heart works harder to
compensate.
3. High blood pressure:
a. Uncontrolled doubles heart failure
risk.
b. Heart pumps harder for circulation.
c. Chamber thickens, becomes weaker
over time.
4. Diabetes and other factors contributing due
to it
a. Tend to have other conditions that
make the heart work harder
b. Diabetes causes damage by scarring
the kidneys, which in turn leads to
salt and water retention, which in
turn raises blood pressure.
c. Over time, diabetes damages the
small blood vessels, causing the
walls of the blood vessels to stiffen
and function improperly. These
changes contribute to high blood
pressure.
d. Obesity
e.
f. High cholesterol
5. Severe anemia
a. Not enough red blood cells to carry
oxygen
b. Heart beats faster and can become
overtaxed with the effort
6. Hyperthyroidism
a. Body metabolism is increased and
overworks the heart
7. Abnormal Heart Rhythm
a. If the heart beats too fast, too slow or
irregular it may not be able to pump
enough blood to the body
Signs and Symptoms
● Shortness of Breath (dyspnea): Blood backs
up in lung veins due to heart's inability to
keep up, leading to fluid leakage into lungs.
● dyspnea during activity or rest
● difficulty breathing when lying flat, and
waking up short of breath.
● Persistent Cough or Wheezing WHY?
● Fluid “backs up” in the lungs
● Coughing that produces white or pink blood
tinged sputum - PULMONARY EDEMA
Edema in Heart Failure:
● Decreased blood flow out of weak heart.
● Blood backs up, fluid builds up in tissues.
● Symptoms: swelling in feet, ankles, legs,
● abdomen, weight gain.
Tiredness and Fatigue in Heart Failure:
● Heart can't pump enough blood for body’s
needs
● Blood diverted from non-vital organs to
heart and brain.
● Symptoms: constant tiredness, difficulty
with daily tasks.
Confusion/Impaired Thinking in Heart Failure:
● Changing blood levels of substances like
sodium can lead to confusion.
● Symptoms: memory loss, disorientation,
noticed by relatives/caregivers.
Increased Heart Rate in Heart Failure:
 ● Heart beats faster to compensate for reduced
pumping.
● Symptoms: heart palpitations, feeling of
racing or throbbing heart.
Treatment Options
The more common forms of heart failure cannot be
cured, but can be treated
● Lifestyle changes
● Medications
● Surgery
Medications used to treat Heart Failure
ACE Inhibitors (Angiotensin converting enzyme
inhibitors):
● Prevents conversion of Angiotensin I to
Angiotensin II
● Cornerstone of heart failure therapy.
● Proven to slow heart failure progression.
● Vasodilators: expand blood vessels, reduce
blood pressure and heart's workload.
● Ex. captopril (Capoten, Capozider)
● cilazapril (brand names include Vascase)
● enalapril (brand names include Enalapril,
Innovace, Innozide)
● fosinopril (brand names include Fosinopril,
Staril)
● imidapril (brand names include Tanatril)
Diuretics (water pills) Lifestyles, Fitness and
Rehabilitation
● Prescribed for fluid build up, swelling or
edema
● Cause kidneys to remove more sodium and
water from the bloodstream
● Decreases workload of the heart and edema
● Fine balance – removing too much fluid can
strain kidneys or cause low blood pressure
● Most diuretics remove potassium from the
body- furosemide (Lasix)
○ Potassium pills compensate for the
amount lost in the urine
○ Potassium helps control heart rhythm
and is essential for the normal work
of the nervous system and muscles
Vasodilators
● Cause blood vessel walls to relax
● Occasionally used if patient cannot tolerate
ACE
● Decrease workload of the heart
Digitalis preparations Lifestyles, Fitness and
Rehabilitation - digoxin
● Increases the force of the hearts contractions
● Positive inotropic agent (increase
contractions)
● Negative chronotropic agent (slows the
heartbeat)
● Relieves symptoms
● Slows heart rate and certain irregular heart
beats
Beta -blockers Lifestyles, Fitness and
Rehabilitation – Beta -blockers
● Lower the heart rate and blood pressure
● Decrease the workload of the heart – Blood-
thinners (coumadin) - warfarin - oral
● Used in patients at risk for developing blood
clots in the blood vessels, legs, lung and
heart
● Used in irregular heart rhythms due to risk
of stroke
Surgery and other Medical Procedures
● Not often used in heart failure unless
required
● Coronary artery bypass
● Angioplasty
 ● Valve replacement
● Defibrillator implantation
● Heart transplantation
● Left ventricular assist device (LVAD)
● Administer Oxygen: If oxygen is available,
providing supplemental oxygen can help
improve oxygenation and ease breathing.
However, this should be done under medical
guidance.
● Stay Calm: It's important to remain as calm
as possible and reassure the person
experiencing heart failure. Stress and panic
can worsen the situation.
● Avoid Overexertion: During a critical
situation, the person should avoid any
physical activity or exertion that could strain
their heart further.
● Keep Medical Information Handy: If the
person has a history of heart failure, having
their medical history, list of medications,
and any relevant documents ready can assist
medical professionals in providing
appropriate care.
● Remember, these are general suggestions,
and managing heart failure in a critical
situation requires immediate medical
attention from trained professionals. If
you're not a medical expert, it's best to focus
on providing comfort, keeping the person as
calm as possible, and waiting for emergency
medical services to arrive.
Heart Failure
● Definition: the heart is too weak to pump
efficiently so it can’t provide proper cardiac
output to maintain the body’s metabolic
needs.
● Results on the body: organs and tissues will
suffer from the decreased blood flow,
pressure in the heart increases which over
works the ventricles, body can become
congested with fluids (enter into congestive
heart failure) that can cause life-threatening
complications.
● Note: the left ventricle is the largest of all
four chambers which allows for maximum
pumping power.
Causes of Heart Failure:
● Mainly due to the heart muscle (specifically
the ventricles) becoming damaged or too
stiff.
Remember the mnemonic: Failure
● Faulty heart valves: AV(tricuspid and
mitral) and SL (Aortic and pulmonic) valve
problems (due to congenital issues or
infection (endocarditis) that causes blood to
back flow (regurgitation) or stenosis
(narrowing of the valves that increases
pressure of blood flow through the valves).
This causes the heart to work harder and
become weak over time.
● Arrhythmias: atrial fibrillation or
tachycardia
● Infarction (myocardial)…coronary artery
disease: part of the heart muscle dies due to
a blockage in the coronary arteries…muscle
become ischemic and can die (main cause of
left ventricular systolic dysfunction)
● Lineage (congenital)…family history
● Uncontrolled Hypertension: overtime this
can lead to stiffening of the heart walls
because with untreated HTN the heart has to
work harder and this causes the ventricles to
become stiff.
● Recreational Drug Use (cocaine) or alcohol
abuse
● Envaders (instead of Invaders): viruses or
infections that attack the heart muscle
Types of Heart Failures:
● Left & Right Side Heart Failure (can have
both at the same time as well)
Left-Sided Heart failure: the left side of the heart
cannot pump blood out of the heart efficiently so
blood starts to back-up in the lungs.
● Most common type of heart failure.
● Left-sided heart failure is likely to lead to
right-sided heart failure.
● The left ventricle becomes too weak and
doesn’t squeeze blood out properly….the
heart failure can be either SYSTOLIC OR
DIASTOLIC.
● Systolic: “Left ventricular systolic
dysfunction” remember systolic is the
contraction or “squeezing” phase of the
heart. In systolic dysfunction, there is an
issue with the left ventricle being able to
eject blood properly out of the ventricle and
the organs can’t get all that rich-oxygenated
blood it just received from the lungs.
● Patients will have a low ejection fraction.
 ● What is ejection fraction?
○ Ejection fraction is a calculation
used to determine the severity of
heart failure on the left side.
○ A normal EF is 50% or greater
meaning that more than half of the
blood that fills inside the ventricles is
being pumped out.
○ An EF can be measured with an
echocardiogram, heart cath, nuclear
stress test.
○ An EF of 40% or less is a diagnosis
for heart failure.
● Diastolic: “left ventricular diastolic
dysfunction” remember diastole is the filling
or resting phase of the heart. In diastolic
dysfunction, the ventricle is
● too stiff to allow for normal filling of blood.
Since there isn’t an issue with contraction
but filling, the ejection fraction is usually
normal.
● Left-sided heart failure will present with
PULMONARY Signs and Symptoms.
Right-Sided Heart Failure: the right side of the
heart cannot pump the “used” blood it received
from the body efficiently so it can’t get the blood
back to the lungs to get replenished with oxygen.
● The causes the blood to back up peripherally
(legs, hands, feet, abdomen).
● Right-sided heart failure causes congestion
of blood in the heart and this increases the
pressure in the inferior vena cava (which
normally brings “used” blood back to the
heart for re-oxygenation). This built-up
pressure causes the hepatic veins to become
very congested with blood which leads to
hepatomegaly and swelling peripherally.
● Right-sided heart failure is usually caused
from left-sided heart failure because of the
increased fluid pressure backing up from the
left side to the right. This causes the right
side of the heart to become overworked.
● Other causes: pulmonary heart disease “cor
pulmonale” as a complication from
pulmonary hypertension or COPD.
● Right-sided heart failure presents with
PERPHIERAL SIGNS AND
SYMPTOMS.
Signs and Symptoms of Heart Failure
Left-sided heart failure:
● Remember the mnemonic DROWNING
(these patients are literally drowning in their
own fluid from the heart’s failure to pump
efficiently)
● Difficulty breathing
● Rales (crackles)
● Orthopnea (cannot tolerate lying down…
must sit-up to breath, especially while
sleeping)
● Weakness (extremely tired and fatigued due
to shortness of breath and heart can’t
compensate for increased activity)
● Nocturnal Paroxysmal dyspnea (awaking
during sleep with extreme dyspnea)
● Increased heart rate (due to fluid overload
and the heart is trying to get the blood to
organs but it can’t because of muscle
failure)
● Nagging cough (can be frothy or blood-
tinged sputum from fluid overload in the
lungs…very bad sign) -Pul Edema
● Gaining weight from the body retaining
fluid…2 to 3 lb in a day or 5 lbs in a week
Right-Sided Heart Failure:
● Remember the mnemonic SWELLING
(fluid is backing up in the right side of the
heart which causes fluid to back-up in the
hepatic veins and peripheral veins)
● Swelling of legs, hands, liver, abdomen
● Weight gain
● Edema (pitting)
● Large neck veins (jugular venous distention)
● Lethargic (weak and very tired)
● Irregular heart rate (atrial fibrillation)
● Nocturia (frequent urination at night) lying
down elevates the legs and allows the extra
fluid to enter into the vascular system which
allows the kidneys to eliminate the extra
fluid.
● Girth of abdomen increased (from swelling
of the liver and building up fluid in the
abdomen)…can’t breathe well and this
causes nausea and anorexia.
Tests used to Diagnose Heart Failure:
● BNP (b-type natriuretic peptide) blood test:
a biomarker released by the ventricles when
there is excessive pressure in the heart due
to heart failure.
○ <100 pg/mL no failure
○ 100-300 pg/mL present
○ 300 pg/mL mild
○ 600 pg/mL moderate
○ 900 pg/mL severe
● Chest x-ray
 ● Echocardiogram
● Heart cath
● Nuclear stress test
● Heart failure can be acute or chronic and can
be triggered/exacerbated with:
○ High salt intake or fluid (watch
fluids)
○ Infection
○ Uncontrolled atrial fibrillation
○ Renal failure
○ Administering medications:
Nursing Interventions for Heart Failure
● Role: Assessing, monitoring, intervening,
and educating
Assessing:
● Assess patient for worsening symptoms
(right-sided failure…peripheral swelling vs
left-sided failure…pulmonary edema)
● Patient responsiveness to medication
treatment:
● watch heart rate (Digoxin)
● respiratory status
● blood pressure (vasodilators cause
hypotension)
● diuretics (strict intake and output, daily
weights, monitor electrolyte levels,
especially K+)
Monitoring:
● Fluid status (may be ordered a Foley
catheter, if on diuretics)
● Cardiac diet (low in salt and fats)
● Fluid restriction (no more than 2 L per day)
● Lab values: watching BNP, kidney function
BUN & creatinine, troponins levels,
electrolytes (especially potassium…if on
Lasix: waste potassium and low potassium
increases risk of digoxin toxicity)
● Edema in leg: Keep legs elevated and
patient in high Fowler’s to help with
breathing
● Safety (at risk for falls due to fluid status
changes, swelling in legs and feet, and
orthostatic hypotension)
Educating:
● Early signs and symptoms heart failure
exacerbation
● Shortness of breath
● Weight gain
● Orthopnea
● Low salt (allowed 2-3 G sodium per day)
and fluid restriction (no more than 2 L per
day)
● Vaccination to prevent illness, such as
annual flu and to be up-to-date with
pneumonia vaccine
● Exercise aerobic (as tolerated)
● Daily weights (watch for no more than 2-3
lb per day and 5 lbs per week)
● Compliance with medications
● Smoking cessation
● Limiting alcohol
● Always Administer Drugs Before A
Ventricle Dies!
Ace Inhibitors (angiotensin-converting-enzyme
inhibitors):
● first line of treatment for heart failure with
beta blockers
● end in “pril” Lisinopril, Ramipril, Enalapril,
Captopril
● works by allowing more blood to get to the
heart muscle which allows it to work easier.
● Also, blocks the conversion of Angiotensin I
or Angiotensin II (this causes vasodilation,
lowers blood pressure, allows kidneys to
secrete sodium because it decreases
aldosterone)
● side effects: dry, nagging cough and can
increase potassium (inhibiting angiotensin II
which decreases aldosterone in the body
which causes the body to retain more
potassium and excrete sodium)
ARBs (Angiotensin II receptor blockers):
● end in “sartan” like Losartan, Valsartan
● used in place of ACE inhibitors if patient
can’t tolerate them
● blocks angiotensin II receptors which causes
vasodilation. This lowers blood pressure and
helps the kidneys to excrete sodium and
water (due to the affects that blocking
angiotensin II has on the kidneys…
decreases aldosterone).
● side effects: increases potassium
levels….NO dry nagging cough
Diuretics:
● used along with ACE inhibitors or ARBs to
decrease water and sodium retention which
will decrease edema in the body and lungs.
This allows the heart to pump easier.
● Patients will urinate a lot!
● Loop diuretics (most common) like Lasix or
Furosemide (watch potassium level because
they will waste potassium)
 ● Potassium-sparing diuretics like a negative chronotropic action that causes
“Aldactone” (can cause hyperkalemia, the heart to beat slower
especially if taking with ACE or ARBs) ● So, the heart slows down and contracts
Beta Blockers: stronger which allows the heart to pump
● blocks norepinephrine and epinephrine more blood.
effects on the heart muscle ● treatment for patients with left ventricular
● given in stable heart failure with ACE systolic dysfunction (however, not usually
inhibitors the first line of treatment due to side effects
● end in “lol” like Metoprolol, Carvedilol and and toxicity risks)…used alongside
Bisoprolol ACE/beta blockers, and diuretics
● not for acute heart failure because the ● toxicity issues: monitor patient potassium
negative inotropic effect on the heart level (hypokalemia <3.5 mEq/L) because
(decrease contraction). The negative hypokalemia increases digoxin toxicity
inotropic effect causes decrease myocardial ● S & S of toxicity: nausea, vomiting, visual
contractility (slows heart) and decreases changes yellowish green halos
cardiac work load. ● normal Digoxin range 0.5 to 2 ng/mL
● used in stable heart failure in people with ● not for patients with a second or third degree
ventricular systolic dysfunction (there is a heart block
contraction problem with the left ventricle) ● check apical pulse before giving….>60 bpm
● To treat diastolic heart failure (remember ● antidote: Digibind
there is a problem with the heart filling in
diastolic dysfunction). It will help the heart
rest so the stiff ventricle can fill properly
and the volume of blood pumped out
increases.
● side effects: check pulse (bradycardia), no
grape juice; mask hypoglycemic signs in
diabetics, respiratory issues in asthmatics
and patients with COPD
Anticoagulants:
● not used in all patients with heart failure
● Typically, used in patients with heart failure
who are in a-fib because they are at risk for
blood clot formation or certain scenarios of
left ventricular systolic heart failure when
there is a low ejection fraction of <35%.

Vasodilators:
● (arterial dilator) Hydralazine…prescribed
with a nitrate like Isordil (venous dilator)
● sometimes used in place of an ACE or ARB,
if patient can’t tolerate them
● this causes vasodilation in the arteries and
veins to help decrease the amount of blood
and fluid going back which helps decrease
the work load on the heart
● side effects: low blood pressure, orthostatic
hypotension

Digoxin:
● Positive inotropic effect that increases the
heart’s ability to contract stronger and it has
ACUTE
RESPIRATORY FAILURE
● The exchange of oxygen for CO2 in the
lungs cannot keep up with the rate of
O2 consumption and CO2 production by
the cells of the body.
● There is a sudden and life-threatening
deterioration of the gas exchange function of
the lung.
HEMODYNAMIC MANIFESTATION
● PaO2 of less than 50 mm Hg
● PaCO2 to greater than 50 mm Hg
● pH of less than 7.35
COMMON MANIFESTATION
● Except . . .
● A. hypoxia
● B. hypothermia
● C. hypoxemia
● D. hypercapnia
COMMON CAUSES
Decreased respiratory drive
● Severe brain injury
● Large lesions of the brain stem (multiple
sclerosis)
● Use of sedative medications
● Metabolic disorders such as hypothyroidism.
● MS – demyelination of the nerve fiber of
spinal cord that leads to the failure
transmission of electrical impulses.
● In severe stage of hypothyroidism, patient’s
respiratory drive is depressed, resulting in
alveolar hypoventilation, progressive CO2
retention, narcosis and coma.
● The rhythm of breathing is controlled by
respiratory centers in the brain. The
inspiratory and expiratory centers in the
medulla oblongata and pons control the
rate and depth of ventilation to meet the
body’s metabolic demands.
● The pons contains motor and sensory
pathways. Portions of the pons also control
the heart, respiration, and BP.
Dysfunction of the chest wall
● Myasthenia gravis
○ Destruction of the acetylcholine, an
excitatory neurotransmitter that is
responsible for the tone and strength
of the muscles which could involve
upper extremities that could lead to
respiratory paralysis.
● Poliomyelitis
○ disease affecting brain and spinal
cord: a severe infectious viral
disease, usually affecting children or
young adults, that inflames the
brainstem and spinal cord,
sometimes leading to loss of
voluntary movement and muscular
wasting.
○ dysfunction in the neural pathways
● Guillain-Barré syndrome -demyelination of
the axon/sheath.
● Cervical spinal cord injuries
● Disease or disorder of the nerves, spinal
cord, muscles, or neuromuscular junction
involved in respiration seriously affects
ventilation:
● Injury to the cervical nerve 4-6 and thoracic
nerve 6 can affect ventilation.
Dysfunction of the lung parenchyma,
● Pleural effusion
○ a collection of fluid (5-15ml) in the
pleural space, is rarely a primary
disease process but is usually
secondary to other diseases.
● Hemothorax
● Pneumothorax
● Upper airway obstruction
● Pulmonary embolism
● Pneumonia
● Status asthmaticus
● Lobar atelectasis
● Pulmonary edema.
○ are conditions that interfere with
ventilation by preventing expansion
of the lung.
○ defined as abnormal accumulation of
fluid in the lung tissue and/or
alveolar space.
Other causes
● Major abdominal, cardiac, or thoracic
surgery.
● Effects of anesthetic agents, analgesics,
and sedatives
● Pain
○ Analgesics, and sedatives enhance
the effects of opioids that leads to
hypoventilation.
○ A mismatch of ventilation to
perfusion is the usual cause of
 respiratory failure after a major heart rhythm, sometimes causing you
surgery to feel a skipped beat or palpitations.
● A ventilation-perfusion imbalance occurs
from an inadequate ventilation, inadequate
perfusion or both.

Pathophysiology
● Poor ventilation
● Poor oxygenation
● Rise and fall of Partial Pressures ●
● Lots of lactic acid
● RESPIRATORY FAILURE LABORATORY Exam.
● CBC (Hg and Hct level, WBC)
SIGNS and SYMPTOMS ● Blood cultures
● Restlessness ● Sputum cultures
● Fatigue ● Gram stain
● Headache
● Dyspnea Treatment
● air hunger To restore adequate oxygen and ventilation
● Confusion ● OXYGEN THERAPY
● lethargy ○ ET intubation
● Tachycardia ○ Mechanical ventilation
● increased BP ○ High frequency or pressure
● Tachypnea ventilation
● central cyanosis
● diaphoresis, To correct the underlying cause and
● Cold clammy skin development of RF
● Use of accessory muscles ● DRUG THERAPY
● Decreased breath sounds ○ Naloxone (Narcan) - antidote to
● Adventitious breath sounds opioids
○ Bronchodilators
Diagnostics ○ Antibiotics - pneumonia
● ABG/SpO2 ○ Corticosteroids - anti-inflammatory
○ PaO2 - less than 60 mm Hg ○ IV solutions of positive inotropics
○ PaCO2 - greater than 45 mm Hg (dopa and dobu)
○ HCO3 - normal ○ Diuretics - decrease fluid buildup
○ pH – low
○ Decreased Oxygen saturation NURSING INTERVENTION/MNG’T
● CHEST X-RAY ● Assisting with intubation and maintaining
○ Emphysema mechanical ventilation
○ Atelectasis ● Assesses the patient’s respiratory status by
○ Pneumothorax ○ monitoring the patient’s level of
○ Infiltrates response, arterial blood
○ Effusion gases, pulse oximetry, and v/s
○ A chest X-ray will reveal bilateral ● Prevent complications. ( turning schedule,
infiltrates — when a substance mouth care, skin care, ROM of extremities)
denser than air (e.g., pus, blood, or ● Management strategies that initiates some
protein) accumulates in the lungs. form of communication
● ECG
○ Premature ventricular contractions ● 1 - aspiration pneumonia
(PVCs) are extra, abnormal ● 2 – pulmonary edema
heartbeats that begin in the ● 3 - pneumothorax
ventricles, or lower pumping ● 4 – atelectasis
chambers, and disrupt your regular
ARDS NCLEX Review
● What is ARDS (acute respiratory distress
syndrome)? It’s a type of respiratory failure
that occurs when the capillary membrane
that surrounds the alveoli sac becomes
damaged, which causes fluid to leak into the
alveoli sac.
● Result? Impaired gas exchange! Gas
exchange doesn’t occur properly due to
many reasons, such as: fluid in the alveoli
sac, collapsed alveoli sacs, and a decrease in
lung compliance (hence the lungs are
becoming less elastic….”stiff”).
● This will lead to oxygen not being able to
cross the alveolar capillary membrane to go
back in the blood to oxygenate it, which will
result in hypoxemia. In turn, the organs of
the body will suffer due to this and death
can occur if treatment does not happen. In
majority cases of ARDS, the patient will
need respiratory assistance via a ventilator
with PEEP
Quick Facts about Acute Respiratory Distress
Syndrome (ARDS)
● It has a fast onset!
● It tends to occur in people who are already
sick (hospitalized) and develops as a
complication. For example, a patient who
has experienced severe burns is at risk for
ARDS due to the systemic inflammation
present in the body.
● ARDS has a high mortality rate!
● What can cause the capillary membrane to
become more permeable and leak fluid?
Usually events that lead to major systemic
inflammation in the body, which can
indirectly damage the capillary membrane or
directly damage the capillary membrane.
Indirect vs. Direct Injury to the Capillary
Membrane
Indirect (source isn’t the lungs): the capillary
membrane is INDIRECTLY damaged. There is a
systemic inflammatory response system (SIRS) by
the immune system.
● Common Causes:
○ *Sepsis (most common and there is a
very poor prognosis if the patient has
a gram-negative bacteria)
○ Burns
○ Blood transfusion (multiple)
○ Inflammation of the pancreas
(pancreatitis)
○ Drug overdose
Direct (source is the lungs)….capillary membrane
is DIRECTLY damaged
● Pneumonia
● Aspiration
● Inhaling a toxic substance
● Significant drowning event
● Embolism
Pathophysiology
Exudative Phase: occurs about 24 hours after
injury to the lung (directly or indirectly)
● Damage to the capillary membrane that
leads to pulmonary edema. This causes the
leaking of fluid, proteins, and other
substances into the interstitium and then into
the alveoli sac. It is very important to note
this fluid contains a LOT of protein.
Significance? Remember proteins regulate
water pressure, oncotic pressure! So, if the
fluid is high in protein it’s going to draw
even MORE fluid into the interstitium and
then the alveoli sac.
● Cells that produce surfactant become
overwhelmed and damaged.
○ Role of surfactant: decreases surface
tension in the lungs. In other words,
the alveoli sacs stay stable.
Therefore, when a person exhales the
sac does NOT collapse.
● A decrease in surfactant creates an
unpredictable alveoli sac that can easily
collapse. This leads to:
● ATELETASIS will occur (collapse of the
lung tissue)
● To make matters worse: a membrane that is
made up of dead cells and other substances
start to collect on the alveoli. This is called a
hyaline membrane. This membrane will
continue to develop in the next phase and
will cause the lungs to become LESS elastic
and can further impair gas exchange!
● End Result? With all the fluid in the alveoli
sac (pulmonary edema), development of a
hyaline membrane, collapsing of the sacs,
decreased surfactant = inadequate
ventilation where alveoli sacs are NOT
getting enough air (leading to V/Q
mismatch) AND a hallmark sign and
symptom: REFRACTORY HYPOXEMIA
○ Refractory hypoxemia is where the
patient will maintain a low blood
oxygen level even though they are
receiving high amounts of oxygen!
 ● Early: Due to all this the patient will
experience an increase in breathing (still
have hypoxemia). WHY? The body is trying
to increase the oxygen level, but it won’t be
able to! This will cause the patient to blow
off too much carbon dioxide (CO2 can still
cross the membrane but O2 can’t)
….respiratory ALKALOSIS will develop
BUT in the late phase (as the patient
progresses to the 2nd and 3rd phases (late),
carbon dioxide levels start to rise. This is
because the hyaline membrane continues to
develop leading to carbon dioxide not being
able to cross over to be exhaled, and the
patient will no longer be able to maintain
breathing due to weak respiratory muscles.
Respiratory acidosis will start to develop
later on.
Proliferative Phase: occurs about 14 days after the
injury (grow or reproduce new cells quickly)
● repair structures, fluid in the sac is
reabsorbed, but lung tissue becomes very
dense and fibrous….lung compliance and
hypoxemia becomes even worse
Fibrotic Phase: occurs about 3 weeks after
injury….major fibrosis of the lung tissue, decreases
lung compliance and hypoxemia with dead space
filling the lungs.
● Patients who enter the fibrotic phase will
have major lung damage and poor recovery.
Pathophysiology of ARDS in a Nutshell
● Atelectasis (alveolar sac fill with fluid and
collapse…pulmonary edeam)
● Refractory Hypoxemia
● Decrease in lung compliance (lung aren’t as
elastic or stretchable….hyaline membrane
develops)
● Surfactant cell damaged (decrease in
surfactant production)
Signs and Symptoms of ARDS
● In the very early phase: sign and symptoms
are hard to detect. At first the fluid is leaking
in the interstitum so lung sounds may be
normal or random a crackle here or there.
But as it progresses the patient will have
difficulty breathing and be “air hunger”.
● There will be an increased respiratory rate,
low oxygen in the blood and respiratory
alkalosis.
● Then as time goes on:
Symptoms of full respiratory failure:
● Tachypnea
● difficulty breathing
● major hypoxemia even though receiving a
high about of oxygen (refractory
hypoxemia)
● Cyanosis
● low oxygen saturation
● mental status change (tired, confused),
● Tachycardia
● chest retractions
● decrease lung compliance
● lung sound: crackles throughout, low Pao2,
high PaCo2 x-ray with white-out of bilateral
lung infiltrates
Nursing Interventions for ARDS (acute
respiratory distress syndrome)
Maintain airway/respiratory function:
● Most patients with ARDS will need:
mechanical ventilation with PEEP (positive
end-expiratory pressure)
● The patient will need high amounts of PEEP
because of the collapsed sacs, stiffening of
the lung, and pulmonary edema. Usually the
pressure is anywhere from 10 to 20 cm of
water. This high amount of pressure will
open the sacs, improve gas exchange, and
help keep them clear of fluid.
● Nurse: high PEEP can cause issues with
intrathoracic pressure and decrease cardiac
output (watch out for a low blood pressure)
along with hyperinflation of the lungs
(possible pneumothorax or subq
emphysema…this is where air escapes into
skin from a lung leaking air)
Monitoring ABGs
Positioning to help with respiratory function:
● Prone Positioning: turning the patient from
supine to prone (putting the patient on their
belly)
● This helps improve oxygen levels without
actually giving the patient a high
concentration of oxygen! Remember in this
position the heart will shift forward and not
compress the back of the lungs and it will
help drain areas of the lungs that normally
can’t be drained in the supine position. So,
this will:
● Help with perfusion and ventilation (helping
with correcting the V/Q mismatch)
 ● Help move secretions from other areas that
were fluid filled and couldn’t move in the
supine position
● Help improve atelectasis.
● How does the MD know if this is pulmonary
edema caused by a cardiac issue like heart
failure or due to a leaking capillary
membrane? A pulmonary artery wedge
pressure can help with that!
○ This is where a pulmonary catheter
with a balloon is inserted into the
pulmonary arterial branch
● If the reading is less than 18 mmHg it
indicates ARDS, but if it’s greater than this
number it indicates a cardiac problem.
● Assessing other systems of the body to make
sure they are getting enough oxygen: mental
status, urine output, heart (blood pressure
and cardiac output with PEEP)

Preventing complications
● pressure injury, blood clots, infection related
to ventilator, nutrition, pneumothorax

Administering drugs
● corticosteroids (help with inflammation),
● antibiotics (preventing and treating
infection)
● fluids colloids or crystalloids solutions if
cardiac output decreased along with drugs
like that have an inotropic effect (helps with
heart muscle contraction)
● GI drugs for stress ulcers