Cardiopulmonary Disorders I

Hibbah Alshuwaikhat, MSc, RRT

◦ Respiratory failure is a general term that indicates failure of the lungs to provide adequate
oxygenation or ventilation for the blood.

 Oxygenation failure is a more specific term indicating an arterial oxygen tension

(PaO2) of less than 60 mm Hg despite a fraction of inspired oxygen (FIO2) of 0.50 or
higher.

 Ventilatory failure refers to inadequate ventilation between the lungs and atmosphere
that results in an inappropriate elevation of arterial carbon dioxide tension (PaCO2) of
greater than 45 mm Hg in the arterial blood.
◦ The term respiratory failure may be used in a more general fashion to describe failure of
either external or internal respiration.

◦ For example, if the circulatory system fails to move the blood at a sufficient rate to meet
metabolic demands, the transport of oxygen is inadequate and the tissues may become
hypoxic.
◦ The amount of oxygen consumed and CO2 produced each
minute is dictated by the metabolic rate of the patient.

◦ Exercise and fever are examples of factors that increase the

metabolic rate and place more demands on the
cardiopulmonary system. When the cardiopulmonary reserve
is limited by disease, fever may represent an added stress that
precipitates respiratory failure and tissue hypoxia.
oHypoxemia is present when the PaO2 is below the predicted normal value for a given patient.
Hypoxemia is classified as:

 Mild (PaO2 60 to 79 mm Hg)

 Moderate (PaO2 40 to 59 mm Hg)
 Severe (PaO2 less than 40 mm Hg)

oThis classification is based on predicted normal values for a patient who is less than 60 years
old and breathing room air.
oFor older patients, subtract 1 mm Hg for every year over 60 years of age from the limits of mild
and moderate hypoxemia.
oA PaO2 of less than 40 mm Hg represents severe hypoxemia at any age.
◦ Hypoxemia has potentially serious consequences because it can lead to inadequate tissue
oxygenation (hypoxia).

◦ When hypoxemia is present, tissue oxygenation may be preserved by an increase in cardiac

output. Patients with severe hypoxemia or marginal cardiac function may not be able to
compensate adequately for the hypoxemia, resulting in tissue hypoxia.

◦ Tissue hypoxia of the heart complicates the problem by causing dysrhythmias and poor
contractility, which add to the lack of oxygen delivery throughout the body.
◦ The most common cause of hypoxemia is ventilation-perfusion (V/Q) mismatching, which
occurs when some regions of the lung are poorly ventilated but remain perfused by pulmonary
blood (low V/Q ).

◦ V/Q mismatching also occurs when perfusion of a portion of the lung is reduced or absent
despite adequate ventilation of the affected region (high V/Q).
◦ Shunt is another cause of hypoxemia and refers to the movement of blood from the right side of
the heart to the left side of the heart without coming into contact with ventilated alveoli.
◦ Shunt can be caused by a congenital heart defect (anatomical shunt), which allows the venous
blood to bypass the pulmonary circulation through abnormal channels (e.g., ventricular septal
defect).
◦ The most common cause of shunt, however, is pulmonary disease that results in collapsed or
unventilated alveoli (physiologic shunt). In this situation, blood flow through the affected lung
regions does not participate in gas exchange and may result in severe hypoxemia (PaO2 less
than 40 mm Hg) that does not respond well to oxygen therapy.
◦ Hypoxemia can occur when an individual inhales a gas mixture that does not contain an
adequate partial pressure of oxygen (low PIO2). Breathing gas that lacks adequate oxygen
results in a below-normal PaO2 (arterial hypoxemia). This situation can occur at high
altitude, during fires in an enclosed structure, and in cases of equipment failure while the
patient is attached to a ventilator circuit.
◦ Hypoventilation increases alveolar PCO2 (PaCO2) and decreases alveolar PO2 (PaO2). If the
patient is breathing room air, hypoventilation can result in hypoxemia. Hypoxemia is less
likely if the hypoventilating patient is breathing an elevated FIO2.
Ventilation/perfusion (V/Q) Mismatch

◦ There are regions in healthy lungs where ventilation and perfusion are not evenly matched.
◦ RTs are familiar with this concept through the work of West, which described a high V/Q
ratio at the apex of the lungs and a low ratio at the bases.
◦ This concept can be explained as there being more air than blood at the apexes and more
blood than air at the bases.
◦ Pathologic V/Q mismatch occurs when disease disrupts this balance, and hypoxemia results
◦ Obstructive lung diseases are frequent causes. The bronchospasm, mucous plugging,
inflammation, and premature airway closure that signal asthmatic or emphysematous
exacerbations worsen ventilation and create V/Q mismatch.
◦ Infection, heart failure, and inhalation injury may lead to partially collapsed or fluid-filled
alveoli, also resulting in decreased ventilation and reduced blood O2 levels.
Shunt
◦ Shunt is an extreme version of V/Q mismatch in which there is no ventilation to match perfusion
(V/Q = 0).
◦ About 2% to 3% of the blood supply is shunted via the bronchial and thebesian veins that feed the
lungs and heart; this is normal anatomic shunt.
◦ Pathologic anatomic shunt occurs as a result of right-to-left blood flow through cardiac openings
(e.g., atrial or ventricular septal defects) or in pulmonary arteriovenous malformations.
◦ Physiologic shunt leads to hypoxemia when alveoli collapse or are filled with fluid or exudate.
◦ Common etiologies of physiologic shunting include atelectasis, pulmonary edema, and pneumonia.
◦ In contrast to V/Q mismatch, shunt does not respond to supplemental O2 because the gas-
exchange unit (the alveolus) is not open
Diffusion Impairment
◦ Diffusion refers to movement of gas across the alveolar-capillary membrane along a pressure gradient.
◦ Although diffusion impairment is rarely a cause of significant hypoxemia at rest, its effects become more
pronounced with exercise, which limits the time for gas exchange.
◦ Diffusion impairment in interstitial lung disease (e.g., pulmonary fibrosis, asbestosis, sarcoidosis), in which the
thickening and scarring of the interstitium undermine normal gas exchange, may contribute 20% to 30% of the
widening in the alveolar-arterial O2 gradient during exercise.
◦ Emphysema, with its alveolar destruction, also has subnormal transfer of O2 and CO2 between the alveolus and
the capillary.
◦ Pulmonary vascular abnormalities can also lead to diffusion impairment.
◦ Anemia, pulmonary hypertension, and pulmonary embolus all may reduce capillary blood flow, resulting in
diminished gas transfer.
Decreased Inspired O2

◦ Also clinically uncommon, hypoxemia may develop when the inspired O2 is less than body
requirements.

◦ The most common situation is at high altitude, where hypoxemia occurs not because of a
decrease in the fraction of oxygen in the ambient air (which remains 21%) but from
barometric pressure decreases, which results in a decrease in the partial pressure of inspired
O2.
Venous Admixture
◦ A decrease in mixed venous O2 increases the gradient by which O2 needs to be stepped up as
it passes through the lungs and can contribute to the development of hypoxemia.
◦ Congestive heart failure with low cardiac output is the most common cause of low mixed
venous O2, owing to increased peripheral extraction of O2, and there are therefore other,
more important coexisting determinants of hypoxemia, such as V/Q mismatch and shunting.
◦ Other causes include low hemoglobin concentration and increased O2 consumption. A low
mixed venous O2 may have a significant effect on the ultimate arterial O2 tension in the
presence of lung disease.
◦ The ability to inhale requires a healthy neurological system that stimulates the respiratory
muscles. Contraction of the diaphragm decreases the intrathoracic pressure and causes gas to
flow into the lungs. Minimal effort is required if the chest cage is intact, airways are patent,
and lungs are compliant.

◦ The ability to exhale requires patent airways and a lung parenchyma with sufficient elastic
recoil to hold the bronchioles open until exhalation is complete.
◦ Causes of ventilatory failure include:
◦ Depression of the respiratory center by drugs

◦ Diseases of the brain, spinal cord abnormalities

◦ Muscular diseases

◦ Thoracic cage abnormalities

◦ Upper and lower airway obstruction

◦ A number of factors can contribute to
weakness of the inspiratory muscles causing
acute ventilatory failure.
◦ Malnutrition and electrolyte disturbances
can weaken the ventilatory muscles, and
pulmonary hyperinflation (e.g., emphysema)
can make the diaphragm less efficient. Lung
hyperinflation causes the diaphragm to
assume an abnormally low position that
results in a mechanical disadvantage.
Increased Carbon Dioxide Production
◦ Fever, agitation, exertion, shivering, hypermetabolism, and excess caloric intake all can
result in an increase in VCO2, with consequent hypercapnia in patients with additional
impairment in respiratory control and effector mechanisms.
◦
Impairment in Respiratory Control

◦ Both central (medullary) and peripheral (aortic and carotid bodies) chemoreceptors
responding to CO2 tension and O2 tension stimulate the drive to breathe.
◦ This ventilatory drive can be diminished by various factors, such as drugs (overdose or
sedation), bilateral carotid endarterectomy with incidental resection of the carotid bodies,
brainstem lesions, diseases of the CNS (multiple sclerosis, Parkinson disease, or elevated
intracranial pressure), hypothyroidism, morbid obesity (e.g., obesity-hypoventilation), and
sleep apnea.
◦ Patients at risk of having a decreased ventilatory drive usually can be identified by their
clinical situation (e.g., CNS insult, overdose of sedative medications), and the clinician
should be attentive to reversible causes.
◦ The severity of the hypoxemia and the patient’s preexisting condition determine a
patient’s response to hypoxemia. A previously healthy patient will be unaffected by
mild hypoxemia. A patient with severe cardiopulmonary disease, however, is likely to
be in danger if oxygenation further deteriorates.
◦ Patients usually respond to hypoxemia by increasing their rate of breathing
(tachypnea).
◦ Tachypnea increases minute ventilation, decreases PaCO2, and to some extent
increases PaO2.
◦ Since anatomical dead space (parts of the lung that are ventilated but not perfused) is
fixed, tachypnea represents a major increase in the work of breathing. If the patient’s
respiratory system is unhealthy, as in obstructed airway disease, tachypnea may
represent a serious increase in the work of breathing.
◦ Hypoxemia stimulates the pulmonary capillaries to constrict in the affected regions
(pulmonary vasoconstriction) causing hypoxemia is prevalent throughout the lungs.
◦ Pulmonary vascular resistance (PVR) is increased when pulmonary vasoconstriction
is present.
◦ This increases right heart workload and, if it continues for many months, can result in
right ventricular failure.
◦ Right heart failure is characterized by increased pressure and dilation of the right heart
chamber (as the heart pumps against the constricted capillaries).
◦ The combination of lung disease and right heart failure is known as Cor pulmonale.
◦ Cardiac rate and strength of contraction increase to compensate for hypoxemia.
◦ If coronary artery disease is present, the increased cardiac workload can lead to
ischemia and irreversible damage (infarction).
◦ If the hypoxemia is severe or the heart cannot provide a sufficient increase in cardiac
output to maintain adequate oxygen transport, the brain may be affected, resulting in a
diminished sensorium and cognitive function.
◦ If the brain continues to be hypoxic, the patient will lose consciousness.
◦ Ventilatory failure is defined as a change in respiration resulting in an elevated PaCO2.
◦ Since CO2 is an acid substance in the blood, an acute increase in PaCO2 decreases
arterial blood pH. The combination of an elevated PaCO2 and acidosis severe enough
to drop the pH below 7.20 may have a profound effect on the body.
◦ Ventilatory failure with rising PaCO2 affects the brain much like an anesthetic and
results in somnolence and eventually coma.
 Chronic Respiratory Failure
(Type 1 and Type 2)

◦ For some patients with pulmonary disease and respiratory failure, the condition has
developed over weeks to months to years and has become a chronic state, allowing
compensatory adaptive mechanisms to develop.
◦ Most commonly, chronic hypercapnic respiratory failure accompanying COPD or
obesity-hypoventilation syndrome elicits a renal response, and the kidneys retain
bicarbonate to elevate the blood pH. However, this compensatory metabolic alkalosis
would not be expected to restore the pH to normal.
◦ Inspection of the patient with severe hypoxemia typically reveals central cyanosis
unless anemia is present and obscures the cyanosis.
◦ Central cyanosis is seen as a bluish discoloration of the tongue and mucous
membranes.
◦ Anemia reduces the ability of clinicians to detect cyanosis because the bluish
discoloration of tissues is due to desaturation of the hemoglobin.
◦ Vital signs are typically abnormal, revealing
tachycardia, tachypnea, and hypertension.
◦ Severe acute hypoxemia may leave the
patient confused, agitated, and slow to
respond.
◦ Abnormal cardiac rhythms are common
when severe hypoxemia is present.
◦ If the hypoxemia is chronic, cor pulmonale
may develop causing hepatomegaly, JVD,
and pedal edema.
◦ Laboratory abnormalities associated with hypoxemia include low PaO2, SaO2, and
arterial oxygen content on arterial blood gas (ABG) analysis.
◦ If the hypoxemia is chronic, the bone marrow is stimulated to produce red blood cells,
which results in polycythemia, (increased hemoglobin and hematocrit).
◦ When the hemoglobin increase is significant, the oxygen content of the arterial blood
may be normal or near normal despite the presence of hypoxemia.
◦ Diseases of the lung that cause oxygenation failure usually also cause abnormalities
on the chest radiograph.
◦ Typical abnormalities include infiltrates consistent with pulmonary edema, adult
respiratory distress syndrome (ARDS), atelectasis, or pneumonia.
◦ When the primary cause of the hypoxemia is outside the lung (e.g., shunting from a
congenital heart defect), the chest radiograph is often normal unless a complicating
respiratory problem is present.
◦ Clinical findings that suggest ventilatory failure include headache, diminished
alertness, warm and flushed skin, and bounding peripheral pulses.
◦ These findings are very nonspecific, as they occur in a variety of conditions other than
ventilatory failure.
◦ Since hypoxemia is often present in the patient with ventilatory failure, the clinical
signs of inadequate oxygenation are often simultaneously present.
◦ Hypothermia and loss of consciousness are common when the ventilatory failure is
the result of an overdose of sedatives.
◦ Tricyclic antidepressants frequently increase heart rate and blood pressure and
increase anticholinergic signs (such as hyperthermia, flushing, dilated pupils,
intestinal ileus, and urinary retention).
◦ Breath sounds are often clear in the presence of drug overdose unless aspiration has
occurred.
◦ Aspiration is more likely to occur when sedatives and alcohol are abused (because of
a diminished gag reflex) and may result in crackles in the lower lobes, with a
predominance in the right lower lobe.
◦ The clinical signs of diaphragm fatigue provide an early warning of respiratory failure in the
patient with respiratory distress. It strongly suggests that the patient is in need of ventilatory
assistance.
◦ Fatigue of the diaphragm initially results in tachypnea. This is followed by periods of
respiratory alternans or abdominal paradox.
◦ Respiratory alternans is the short-term alternation between using the diaphragm for breathing
and using the accessory muscles.
◦ Abdominal paradox is the inward movement of the abdomen with each inspiratory effort.
◦ This is due to the flaccid status of the diaphragm, which results in its being drawn upward
when the accessory muscles create a negative intrathoracic pressure .
◦ ABGs are very helpful for assessing the patient with ventilatory failure.
◦ The severity of ventilatory failure is indicated by the degree to which the PaCO2
increases.
◦ Measurement of arterial pH identifies the degree of respiratory acidosis present and
suggests the level of urgency at which treatment needs to be implemented.
◦ The patient needs immediate care when the pH drops below 7.20.
◦ Elevation of FIO2 is the initial treatment for hypoxemia.
◦ Oxygen supplementation rapidly corrects hypoxemia associated with V/Q mismatching or
hypoventilation.
◦ Oxygen therapy in this situation can be given by nasal cannula, simple mask, or entrainment
mask.
◦ The entrainment mask delivers a specific FIO2 regardless of the patient’s breathing pattern.
This is in contrast to the nasal cannula and simple mask, which allow the inhaled FIO2 to
vary with the patient’s respiratory rate and tidal volume.
◦ Hypoxemia caused by either anatomical or physiologic shunting is usually not
responsive to increases in FIO2 because blood traversing the shunt does not come into
contact with ventilated alveoli.
◦ Treatment of anatomical shunt requires closure of the defect, if possible.
◦ Treatment of physiologic shunt requires reopening of alveoli.
◦ Shunt caused by collapse of alveoli often responds to positive pressure ventilation
(PPV). PPV can decrease the patient’s work of breathing and open collapsed alveoli to
allow better gas exchange.
◦ Positive pressure ventilation is generally used to treat hypoxemia when
the patient has a PaO2 of less than 60 mm Hg despite an increase in the
FIO2 to 0.50 or higher.
◦ The application of continuous positive airway pressure (CPAP) by mask is
an acceptable temporary measure as long as ventilation is adequate and
the patient’s problem is likely to resolve quickly (e.g., postoperative
atelectasis).
◦ Intubation and mechanical ventilation are needed if mask CPAP is not
successful in correcting the hypoxemia and reducing the patient’s work of
breathing or when the problem is not likely to resolve quickly (e.g.,
ARDS).
◦ An acute elevation in PaCO2 indicates that the patient is unable to maintain adequate
alveolar ventilation and may be in need of ventilatory assistance.
◦ The PaCO2 does not necessarily have to be above normal range to indicate the need
for mechanical ventilation in all circumstances.
◦ For example, if an asthmatic patient is in acute respiratory distress and the PaCO2
increases from 30 to 40 mm Hg because of muscle fatigue, the patient would benefit
from intubation and mechanical ventilation. This example illustrates how trends in the
PaCO2 can be helpful in determining the need for mechanical ventilation.
Case Study