BLOOD GAS AND ACID-BASE ANALYSIS

1. What are the normal arterial blood gas values in a healthy patient breathing
room air at sea level?
See Table 3-1.
2. What information does arterial blood gas provide about the patient?
Arterial blood gas (ABG) provides an assessment of the following:
n Oxygenation (PaO2). The PaO2 is the amount of oxygen dissolved in the blood and
therefore provides initial information on the efficiency of oxygenation.
n Ventilation (PaCO2). The adequacy of ventilation is inversely proportional to the PaCO2
so that, when ventilation increases, PaCO2 decreases, and when ventilation decreases,
PaCO2 increases.
n Acid-base status (pH, HCO3
, and base deficit [BD]). A plasma pH of >7.4 indicates
alkalemia, and a pH of <7.35 indicates acidemia. Despite a normal pH, an underlying
acidosis or alkalosis may still be present.
Oxygenation and ventilation were discussed in Chapter 2 and acid-base status will be the area
of focus for this chapter.
3. How is the regulation of acid-base balance traditionally described?
Acid-base balance is traditionally explained using the Henderson-Hasselbalch equation, which
states that changes in HCO3
and PaCO2 determine pH as follows:
pH ¼ pK þ log½HCO3=ð0:03 PaCO2Þ
To prevent a change in pH, any increase or decrease in the PaCO2 should be accompanied
by a compensatory increase or decrease in the HCO3
. The importance of other
physiologic nonbicarbonate buffers was later recognized and partly integrated into the
BD and the corrected anion gap, both of which aid in interpreting complex acid-base
disorders.
TABLE 3-1. A R T E R I A L B L O O D G A S V A L U E S A T S E A L E V E L
pH 7.36–7.44
PaCO2 33–44 mm Hg
PaO2 75–105 mm Hg
HCO3 20–26 mmol/L
Base deficit þ3 to 3 mmol/L
SaO2 95%–97%
24
KEY POINTS: MAJOR CAUSES OF AN ANION GAP
METABOLIC ACIDOSIS
Elevated anion gap metabolic acidosis is caused by accumulation of unmeasured anions:
n Lactic acid
n Ketones
n Toxins (ethanol, methanol, salicylates, ethylene glycol, propylene glycol)
n Uremia
4. What is the physiochemical approach (Stewart model) for the analysis of
acid-base balance?
In 1981 Stewart proposed a conceptually different model for analyzing acid-base disorders.
His method used two important principles of solution chemistry: the conservation of mass, and
electroneutrality. He described three independent variables that determine the pH in the
extracellular fluid. These variables are the strong ion difference (SID), the PaCO2, and
the concentration of weak acids (AToT). The SID is calculated as follows with the normal
value given:
SID ¼ ð½Na
þ þ ½K
þ þ ½Ca2þ þ ½Mg2þ Þ ð½Cl
þ ½other anions Þ ¼ 40 42 mEq=L
The concentration of other anions consists of protiens and weak acids. The primary weak acids
in the plasma are proteins (primarily albumin), phosphate, and sulfate. In pathologic states
other weak acids might include lactate, ketones, or toxins. As anions accumulate, the SID
decreases, resulting in an acidosis. If the balance shifts to a predominance of cations, an
alkalosis develops. Stewart developed several equations to show that these parameters were
independent variables and showed that HCO3
and pH were dependent on the three independent
variables, contrary to the Henderson-Hasselbalch and standard base excess approaches. This
model has been most useful in interpreting complex acid-base disorders in patients with mixed
acid-base disorders and disorders that were not observable with conventional acid-base analysis
such as hypoalbuminemia and hyperchloremic metabolic acidosis.
5. What are the common acid-base disorders and their compensation?
See Table 3-2.
TABLE 3-2. MA J O R A C I D - B A S E D I S O R D E R S A N D C OMP E N S A T O R Y ME C H A N I SMS *
Primary Disorder Primary Disturbance Primary Compensation
Respiratory acidosis " PaCO2 " HCO3
Respiratory alkalosis # PaCO2 # HCO3
Metabolic acidosis # HCO3 # PaCO2
Metabolic alkalosis " HCO3 " PaCO2
*Primary compensation for metabolic disorders is achieved rapidly through respiratory control of CO2,
whereas primary compensation for respiratory disorders is achieved more slowly as the kidneys
excrete or absorb acid and bicarbonate. Mixed acid-base disorders are common.
CHAPTER 3 BLOOD GAS AND ACID-BASE ANALYSIS 25
6. How do you calculate the degree of compensation?
See Table 3-3.
7. What are the common causes of respiratory acid-base disorders?
n Respiratory alkalosis: Sepsis, hypoxemia, anxiety, pain, and central nervous system
lesions
n Respiratory acidosis: Drugs (residual anesthetics, residual neuromuscular blockade,
benzodiazepines, opioids), asthma, emphysema, obesity-hypoventilation syndromes,
central nervous system lesions (infection, stroke), and neuromuscular disorders
8. What are the major buffering systems of the body?
Bicarbonate, albumin, intracellular proteins, and phosphate are the major buffering systems.
The extracellular bicarbonate system is the fastest to respond to pH change but has less total
capacity than the intracelluar systems, which account for 60% to 70% of the chemical buffering of
the body. Hydrogen ions are in dynamic equilibrium with all buffering systems of the body.
CO2 molecules also readily cross cell membranes and keep both intracellular and extracellular
buffering systems in dynamic equilibrium. In addition, CO2 has the advantage of excretion through
ventilation.
9. What organs play a major role in acid-base balance?
n The lungs are the primary organ involved in rapid acid-base regulation. Carbon dioxide
produced in the periphery is transported to the lung, where the low carbon dioxide
tension promotes conversion of bicarbonate to carbon dioxide, which is then eliminated.
The respiratory regulatory system can increase and decrease minute ventilation to
compensate for metabolic acid-base disturbances.
n The kidneys act to control acid-base balance by eliminating fixed acids and to control
the elimination of electrolytes, bicarbonate, ammonia, and water.
TABLE 3-3. C A L C U L A T I N G T H E D E G R E E O F C OMP E N S A T I O N *
Primary Disorder Rule
Respiratory acidosis (acute) HCO3
increases 0.1 (PaCO2 40)
pH decreases 0.008 (PaCO2 40)
Respiratory acidosis (chronic) HCO3
increases 0.4 (PaCO2 40)
Respiratory alkalosis (acute) HCO3
decreases 0.2 (40 PaCO2)
pH increases 0.008 (40 PaCO2)
Respiratory alkalosis (chronic) HCO3
decreases 0.4 (40 PaCO2)
Metabolic acidosis PaCO2 decreases 1 to 1.5 (24 HCO3
)
Metabolic alkalosis PaCO2 increases 0.25 to 1 (HCO3
24)
*Compensatory mechanisms never overcorrect for an acid-base disturbance; when ABG analysis
reveals apparent overcorrection, the presence of a mixed disorder should be suspected.
Data from Schrier RW: Renal and electrolyte disorders, ed 3, Boston, 1986, Little, Brown.
26 CHAPTER 3 BLOOD GAS AND ACID-BASE ANALYSIS
n The liver is involved in multiple reactions that result in the production or metabolism
of acids.
n The gastrointestinal tract secretes acidic solutions in the stomach, and absorbs water
and other electrolytes in the small and large intestines. This can have a profound effect in
acid-base balance.
10. What is meant by pH?
pH is the negative logarithm of the hydrogen ion concentration ([Hþ]). pH is a convenient
descriptor for power of hydrogen. Normally the [Hþ] in extacellular fluid is 40 nmol/L, a very
small number. By taking the negative log of this value we obtain a pH of 7.4, a much
simpler way to describe [Hþ]. The pH of a solution is determined by a pH electrode that
measures the [Hþ].
11. Why is pH important?
pH is important because hydrogen ions react highly with cellular proteins, altering their
function. Avoiding acidemia and alkalemia by tightly regulating hydrogen ions is essential for
normal cellular function. Deviations from normal pH suggest that normal physiologic
processes are in disorder and the causes should be determined and treated.
12. List the major consequences of acidemia.
Severe acidemia is defined as blood pH <7.20 and is associated with the following
major effects:
n Impairment of cardiac contractility, cardiac output, and the response to
catecholamines
n Susceptibility to recurrent arrhythmias and lowering the threshold for ventricular
fibrillation
n Arteriolar vasodilation resulting in hypotension
n Vasoconstriction of the pulmonary vasculature, leading to increased pulmonary vascular
resistance
n Hyperventilation (a compensatory response)
n Confusion, obtundation, and coma
n Insulin resistance
n Inhibition of glycolysis and adenosine triphosphate synthesis
n Hyperkalemia as potassium ions are shifted extracellularly
13. List the major consequences of alkalemia.
Severe alkalemia is defined as blood pH >7.60 and is associated with the following
major effects:
n Increased cardiac contractility until pH >7.7, when a decrease is seen
n Refractory ventricular arrhythmias
n Coronary artery spasm/vasoconstriction
n Vasodilation of the pulmonary vasculature, leading to decreased pulmonary vascular
resistance
n Hypoventilation (which can frustrate efforts to wean patients from mechanical ventilation)
n Cerebral vasoconstriction
CHAPTER 3 BLOOD GAS AND ACID-BASE ANALYSIS 27
n Neurologic manifestations such as headache, lethargy, delirium, stupor, tetany, and
seizures
n Hypokalemia, hypocalcemia, hypomagnesemia, and hypophosphatemia
n Stimulation of anaerobic glycolysis and lactate production
14. Is the HCO3 value on the arterial blood gas the same as the CO2 value on the
chemistry panel?
No. The HCO3
is a calculated value, whereas the CO2 is a measured value. Because the CO2 is
measured, it is thought to be a more accurate determination of HCO3
. The ABG HCO3
is
calculated using the Henderson-Hasselbalch equation and the measured values of pH and
PaCO2. In contrast, a chemistry panel reports a measured serum carbon dioxide content (CO2),
which is the sum of the measured bicarbonate (HCO3
) and carbonic acid (H2CO3). The CO2 is
viewed as an accurate determination of HCO3
because the HCO3
concentration in blood is
about 20 times greater than the H2CO3 concentration; thus H2CO3 is only a minor contributor
to the total measured CO2.
15. What is the base deficit? How is it determined?
The BD (or base excess) is the amount of base (or acid) needed to titrate a serum pH back
to normal at 37 C while the PaCO2 is held constant at 40 mm Hg. The BD represents
only the metabolic component of an acid-base disorder. The ABG analyzer derives the BD
from a nomogram based on the measurements of pH, HCO3
, and the nonbicarbonate
buffer hemoglobin. Although the BD is determined in part by the nonbicarbonate buffer
hemoglobin, it is criticized because it is derived from a nomogram and assumes
normal values for other important nonbicarbonate buffers such as albumin. Thus in a
hypoalbuminemic patient the BD should be used with caution since it may conceal an
underlying metabolic acidosis.
16. What is the anion gap?
The anion gap (AG) estimates the presence of unmeasured anions. Excess inorganic
and organic anions that are not readily measured by standard assays are termed unmeasured
anions. The AG is a tool used to further classify a metabolic acidosis as an AG metabolic
acidosis (elevated AG) or a non-AG metabolic acidosis (normal AG). This distinction narrows
the differential diagnosis. The AG is the difference between the major serum cations and anions
that are routinely measured:
AG ¼ Na
þ ðHCO

3
þ Cl
Þ
A normal value is 12 mEq/L 4 mEq/L. When unmeasured acid anions are present, they are
buffered by HCO3
, thereby decreasing the HCO3
concentration. According to the previous
equation, this decrease in HCO3
will increase the AG. Keep in mind that hypoalbuminemia has
an alkalinizing effect that lowers the AG, which may mask an underlying metabolic acidosis
caused by unmeasured anions. This pitfall can be avoided by correcting the AG when
evaluating a metabolic acidosis in a hypoalbuminemic patient:
Corrected AG ¼ observed AG þ 2:5 ðnormal albumin observed albuminÞ
28 CHAPTER 3 BLOOD GAS AND ACID-BASE ANALYSIS
KEY POINTS: MAJOR CAUSES OF A NONANION
GAP METABOLIC ACIDOSIS
Nonanion gap metabolic acidosis results from loss of Naþ and Kþ or accumulation of Cl . The
result of these processes is a decrease in HCO3
:
n Iatrogenic administration of hyperchloremic solutions (hyperchloremic metabolic acidosis)
n Alkaline gastrointestinal losses
n Renal tubular acidosis
n Ureteric diversion through ileal conduit
n Endocrine abnormalities
17. List the common causes of a metabolic alkalosis.
Metabolic alkalosis is commonly caused by vomiting, volume contraction (diuretics,
dehydration), alkali administration, and endocrine disorders.
18. List the common causes of elevated and nonelevated anion gap metabolic
acidosis.
n Nonelevated AG metabolic acidosis is caused by iatrogenic administration of
hyperchloremic solutions (hyperchloremic metabolic acidosis), alkaline gastrointestinal
losses, renal tubular acidosis (RTA), or ureteric diversion through ileal conduit. Excess
administration of normal saline is a cause of hyperchloremic metabolic acidosis.
n Elevated AG metabolic acidosis is caused by accumulation of lactic acid or ketones,
poisoning from toxins (e.g., ethanol, methanol, salicylates, ethylene glycol, propylene
glycol) or uremia.
19. Describe a stepwise approach to acid-base interpretation.
n Check the pH to determine acidemia or alkalemia.
n If the patient is breathing spontaneously, use the following rules:
□ If the PCO2 is increased and the pH is <7.35, the primary disorder is most likely a
respiratory acidosis.
□ If the PCO2 is decreased and the pH >7.40, the primary disorder is most likely a
respiratory alkalosis.
□ If the primary disorder is respiratory, determine if it is acute or chronic.
□ If the PCO2 is increased and the pH is >7.40, the primary disorder is most likely a
metabolic alkalosis with respiratory compensation.
□ If the PCO2 is decreased and the pH <7.35, the primary disorder is most likely
a metabolic acidosis with respiratory compensation.
n Metabolic disorders can also be observed by analyzing the base excess or BD.
□ If there is a metabolic acidosis, calculate the AG and determine if the acidosis is a non-
AG or AG acidosis, remembering to correct for hypoalbuminemia.
□ If the patient is mechanically ventilated or if the acid-base disorder doesn’t seem to make
sense, check electrolytes, albumin, and consider calculating the SID. Also consider the
clinical context of the acid-base disorder (e.g., iatrogenic fluid administration, massive
blood resuscitation, renal failure, liver failure, diarrhea, vomiting, gastric suctioning, toxin
ingestion). This may require further testing, including measuring urine electrolytes,
serum, and urine osmolality, and identifying ingested toxins.

RESPIRATORY AND PULMONARY PHYSIOLOGY

1. What is the functional residual capacity? What factors affect it?
The functional residual capacity (FRC) is the volume in the lungs at the end of passive
expiration. It is determined by opposing forces of the expanding chest wall and the elastic
recoil of the lung. A normal FRC ¼ 1.7 to 3.5 L. FRC is increased by:
n Body size (FRC increases with height)
n Age (FRC increases slightly with age)
n Certain lung diseases, including asthma and chronic obstructive pulmonary disease (COPD).
FRC is decreased by:
n Sex (woman have a 10% decrease in FRC when compared to men)
n Diaphragmatic muscle tone (individuals with paralyzed diaphragms have less FRC when
compared to normal individuals)
n Posture (FRC greatest standing > sitting > prone > lateral > supine)
n Certain lung diseases in which elastic recoil is diminished (e.g., interstitial lung disease,
thoracic burns, and kyphoscoliosis)
n Increased abdominal pressure (e.g., obesity, ascites)
2. What is closing capacity? What factors affect the closing capacity? What is the
relationship between closing capacity and functional residual capacity?
Closing capacity is the point during expiration when small airways begin to close. In young
individuals with average body mass index, closing capacity is approximately half the FRC when
upright and approximately two thirds of the FRC when supine.
Closing capacity increases with age and is equal to FRC in the supine individual at
approximately 44 years and in the upright individual at approximately 66 years. The FRC
depends on position; the closing capacity is independent of position. Closing capacity
increases with increasing intraabdominal pressure, age, decreased pulmonary blood flow, and
pulmonary parenchymal disease, which decreases compliance.
3. What muscles are responsible for inspiration and expiration?
The respiratory muscles include the diaphragm, internal and external intercostals, abdominal
musculature, cervical strapmuscles, sternocleidomastoidmuscle, and large back and intervertebral
muscles of the shoulder girdle. During normal breathing inspiration requires work, whereas
expiration is passive. The diaphragm, scalene muscles, and external intercostal muscles provide
most of the work during normal breathing. However, as the work of breathing increases, abdominal
musculature and internal intercostal muscles become active during expiration, and the scalene and
sternocleidomastoid muscles become increasingly important for inspiration.
4. What is the physiologic work of breathing?
The physiologic work of breathing involves the work of overcoming the elastic recoil of the
lung (compliance and tissue resistance work) and the resistance to gas flow. The elastic recoil
is altered in certain pathologic states, including pulmonary edema, pulmonary fibrosis, thoracic
burns, and COPD. The resistance to gas flow is increased dramatically during labored
breathing. In addition to the physiologic work of breathing, a patient on a ventilator must also
overcome the resistance of the endotracheal tube.
17
5. Discuss the factors that affect the resistance to gas flow. What is laminar and
turbulent gas flow?
The resistance to flow can be separated into the properties of the tube and the properties of
the gas. At low flow, or laminar flow (nonobstructed breathing), the viscosity is the major
property of the gas that affects flow. Clearly the major determining factor is the radius of the
tube. This can be shown by the Hagen-Poiseuille relationship:
R ¼ ð8 L mÞ=ðp r4Þ
where R is resistance, L is the length of the tube, m is the viscosity, and r is the radius of the
tube. At higher flow rate (in obstructed airways and heavy breathing), the flow is turbulent.
At these flows the major determinants of resistance to flow are the density of the gas (r) and
the radius of the tube, r.
Ra r=r5
6. Suppose a patient has an indwelling 7-mm endotracheal tube and cannot be
weaned because of the increased work of breathing. What would be of greater
benefit, cutting off 4 cm of endotracheal tube or replacing the tube with one of
greater internal diameter?
According to the Hagen-Poiseuille relationship discussed previously, if the radius is
halved, the resistance within the tube increases to sixteenfold; but if the length of the tube is
doubled, the resistance is only doubled. Cutting the length of the tube minimally
affects resistance, but increasing the tube diameter dramatically decreases resistance.
Therefore, to reduce the work of breathing the endotracheal tube should be changed to a
larger size.
7. Why might helium be of benefit to a stridorous patient?
When flow is turbulent, as is the case in a stridorous patient, driving pressure is mostly
related to gas density. Use of low-density gas mixtures containing helium and oxygen lowers
the driving pressure needed to move gas in and out of the area, decreasing the work of
breathing.
8. Discuss dynamic and static compliance.
Compliance describes the elastic properties of the lung. It is a measure of the change in
volume of the lung when pressure is applied. The lung is an elastic body that exhibits elastic
hysteresis. When the lung is rapidly inflated and held at a given volume, the pressure
peaks and then exponentially falls to a plateau pressure. The volume change of the lung per the
initial peak pressure change is the dynamic compliance. The volume change per the plateau
pressure represents the static compliance of the lung.
9. How does surface tension affect the forces in the small airways and alveoli?
Laplace’s law describes the relationship between pressure (P), tension (T), and the radius
(R) of a bubble and can be applied to the alveoli.
P ¼ 2T=R
As the radius decreases, the pressure increases. In a lung without surfactant present, as
the alveoli decrease in size, the pressure is higher in small alveoli, causing gas to move from
the small to larger airways, collapsing in the process. Surfactant, a phospholipid substance
produced in the lung by type II alveolar epithelium, reduces the surface tension of the small
airways, thus decreasing the pressure as the airways decrease in size. This important
substance helps keep the small airways open during expiration.
18 CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY
10. Review the different zones (of West) in the lung with regard to perfusion and
ventilation.
West described three areas of perfusion in an upright lung, and a fourth was later added.
Beginning at the apices, they are:
n Zone 1: Alveolar pressure (PAlv) exceeds pulmonary artery pressure (Ppa) and pulmonary
venous pressure (Ppv), leading to ventilation without perfusion (alveolar dead space) (PAlv
> Ppa > Ppv).
n Zone 2: Pulmonary arterial pressure exceeds alveolar pressure, but alveolar pressure still
exceeds venous pressure (Ppa > PAlv > Ppv). Blood flow in zone 2 is determined by
arterial-alveolar pressure difference.
n Zone 3: Pulmonary venous pressure exceeds alveolar pressure, and flow is determined
by the arterial-venous pressure difference (Ppa > Ppv >PAlv).
n Zone 4: Interstitial pressure (Pinterstitium) is greater than venous and alveolar pressures;
thus flow is determined by the arterial-interstitial pressure difference (Ppa > Pinterstitium >
Ppv > PAlv). Zone 4 should be minimal in a healthy patient.
A change from upright to supine position increases pulmonary blood volume by 25% to
30%, thus increasing the size of larger-numbered West zones.
11. What are the alveolar gas equation and the normal alveolar pressure at sea
level on room air?
The alveolar gas equation is used to calculate the alveolar oxygen partial pressure:
PAO2 ¼ FiO2 ðPB PH2OÞ PaCO2=RQ
where PAO2 is the alveolar oxygen partial pressure, FiO2 is the fraction of inspired oxygen,
Pb is the barometric pressure, PH2O is the partial pressure of water (47mmHg), PaCO2 is the partial
pressure of carbon dioxide, and RQ is the respiratory quotient, dependent on metabolic activity and
diet and is considered to be about 0.825. At sea level the alveolar partial pressure (PAO2) is:
PaO2 ¼ 0:21ð760 47Þ 40=0:8 ¼ 99:7
Knowing the PaO2 allows us to calculate the alveolar-arterial O2 gradient (A-a gradient).
Furthermore, by understanding the alveolar gas equation we can see how hypoventilation
(resulting in hypercapnia) lowers PaO2, and therefore PaO2.
12. What is the A-a gradient and what is a normal value for this gradient?
The alveolar-arterial O2 gradient is known as the A-a gradient. It is the difference in partial
pressure of O2 in the alveolus (PaO2), calculated by the alveolar gas equation, and the partial
pressure of O2 measured in the blood (PaO2):
A-a gradient = PaO2 PaO2
A normal A-a gradient is estimated as follows:
A-a gradient = (age/4) þ 4.
13. What is the practical significance of estimating A-a gradient?
The A-a gradient, together with the PaO2 and PaCO2, allows systematic evaluation of
hypoxemia, leading to a concise differential diagnosis. As previously stated, the ABG provides
an initial assessment of oxygenation by measuring the PaO2. The A-a gradient is an extension
of this, for by calculating the difference between the PaO2 and the PaO2 we are assessing
the efficiency of gas exchange at the alveolar-capillary membrane.
14. What are the causes of hypoxemia?
n Low inspired oxygen concentration (FiO2): To prevent delivery of hypoxic gas mixtures
during an anesthetic, oxygen alarms are present on the anesthesia machine.
CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY 19
n Hypoventilation: Patients under general anesthesia may be incapable of maintaining an
adequate minute ventilation because of muscle relaxants or the ventilatory depressant
effects of anesthetic agents. Hypoventilation is a common problem after surgery.
n Shunt: Sepsis, liver failure, arteriovenous malformations, pulmonary emboli, and right-toleft
cardiac shunts may create sufficient shunting to result in hypoxemia. Since shunted
blood is not exposed to alveoli, hypoxemia caused by a shunt cannot be overcome by
increasing FiO2.
n Ventilation-perfusion (V/Q) mismatch: Ventilation and perfusion of the alveoli in the lung
ideally have close to a one-to-one relationship, promoting efficient oxygen exchange
between alveoli and blood. When alveolar ventilation and perfusion to the lungs are unequal
(V/Q mismatching), hypoxemia results. Causes of V/Q mismatching include atelectasis,
lateral decubitus positioning, bronchial intubation, bronchospasm, pneumonia, mucous
plugging, pulmonary contusion, and adult respiratory distress syndrome. Hypoxemia
caused by V/Q mismatching can usually be overcome by increasing FiO2.
n Diffusion defects: Efficient O2 exchange depends on a healthy interface between the alveoli
and the bloodstream. Advanced pulmonary disease and pulmonary edema may have
associated diffusion impairment.
KEY POINTS: CAUSES OF HYPOXEMIA
1. Low inspired oxygen tension
2. Alveolar hypoventilation
3. Right-Left shunting
4. V/Q mismatch
5. Diffusion abnormality
15. What are the A-a gradients for the different causes of hypoxemia:
n Low fractional concentration of inspired O2: normal A-a gradient
n Alveolar hypoventilation: normal A-a gradient
n Right-to-left shunting: elevated A-a gradient
n Ventilation/perfusion mismatch: elevated A-a gradient
n Diffusion abnormality: elevated A-a gradient
16. Discuss V/Q mismatch. How can general anesthesia worsen V/Q mismatch?
V/Q mismatch ranges from shunt at one end of the spectrum to dead space at the other end.
In the normal individual alveolar ventilation (V) and perfusion (Q) vary throughout the lung
anatomy. In the ideal situation V and Q are equal, and V/Q ¼ 1. In shunted lung the perfusion is
greater than the ventilation, creating areas of lung where blood flow is high but little gas
exchange occurs. In dead-space lung, ventilation is far greater than perfusion, creating areas of
lung where gas is delivered but little blood flow and gas exchange occur. Both situations
can cause hypoxemia. In the case of dead space, increasing the FiO2 will potentially increase
the hemoglobin oxygen saturation, whereas in cases of shunt it will not. In many pathologic
situations both extremes coexist within the lung.
Under general anesthesia FRC is reduced by approximately 400 ml in an adult. The supine
position decreases FRC another 800 ml. A large enough decrease in FRC may bring end-expiratory
volumes or even the entire tidal volume to levels below the closing volume (the volume at which
small airways close). When small airways begin to close, atelectasis and low V/Q areas develop.
20 CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY
17. Define anatomic, alveolar, and physiologic dead space.
Physiologic dead space (VD) is the sum of anatomic and alveolar dead space. Anatomic dead
space is the volume of lung that does not exchange gas. This includes the nose, pharynx,
trachea, and bronchi. This is about 2 ml/kg in the spontaneously breathing individual and is
the majority of physiologic dead space. Endotracheal intubation will decrease the total
anatomic dead space. Alveolar dead space is the volume of gas that reaches the alveoli but
does not take part in gas exchange because the alveoli are not perfused. In healthy patients
alveolar dead space is negligible.
18. How is VD/VT calculated?
VD/VT is the ratio of the physiologic dead space to the tidal volume (VT), is usually about 33%,
and is determined by the following formula:
VD=VT ¼ ½ðalveolar PCO2 expired PCO2Þ =alveolar PCO2
Alveolar PCO2 is calculated using the alveolar gas equation, and expired PCO2 is the average
PCO2 in an expired gas sample (not the same as end-tidal PCO2).
19. Define absolute shunt. How is the shunt fraction calculated?
Absolute shunt is defined as blood that reaches the arterial system without passing
through ventilated regions of the lung. The fraction of cardiac output that passes through a
shunt is determined by the following equation:
Qs=Qt ¼ ðCiO2 CaO2Þ=ðCiO2 CvO2Þ
where Qs is the physiologic shunt blood flow per minute, Qt is the cardiac output per minute,
CiO2 is the ideal arterial oxygen concentration when V/Q ¼ 1, CaO2 is arterial oxygen
content, and CvO2 is mixed venous oxygen content. It is estimated that 2% to 5% of cardiac
output is normally shunted through postpulmonary shunts, thus accounting for the normal
alveolar-arterial oxygen gradient (A-a gradient). Postpulmonary shunts include the thebesian,
bronchial, mediastinal, and pleural veins.
20. What is hypoxic pulmonary vasoconstriction?
Hypoxic pulmonary vasoconstriction (HPV) is a local response of pulmonary arterial
smooth muscle that decreases blood flow in the presence of low alveolar oxygen pressure,
helping to maintain normal V/Q relationships by diverting blood from under ventilated areas. HPV
is inhibited by volatile anesthetics and vasodilators but is not affected by intravenous anesthesia.
21. Calculate arterial and venous oxygen content (CaO2 and CvO2).
Oxygen content (milliliters of O2/dl) is calculated by summing the oxygen bound to hemoglobin
(Hgb) and the dissolved oxygen of blood:
Oxygen content ¼ 1:34 ½Hgb SaO2 þ ðPaO2 0:003Þ
where 1.34 is the O2 content per gram hemoglobin, SaO2 is the hemoglobin saturation, [Hgb]
is the hemoglobin concentration, and PaO2 is the arterial oxygen concentration.
If [Hgb] ¼ 15 g/dl, arterial saturation ¼ 96%, and PaO2 ¼ 90 mm Hg, mixed venous
saturation ¼ 75%, and PvO2 ¼ 40 mm Hg, then:
CaO2 ¼ ð1:34 ml O2=g Hgb 15 g Hgb=dl 0:96Þ þ ð90 0:003Þ ¼ 19:6 ml O2=dl
and
CvO2 ¼ ð1:34 ml O2=g Hgb 15 g Hgb=dl 0:75Þ þ ð40 0:003Þ ¼ 15:2 ml O2=dl
22. How is CO2 transported in the blood?
CO2 exists in three forms in blood: dissolved CO2 (7%), bicarbonate ions (HCO3
) (70%), and
combined with hemoglobin (23%).
CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY 21
23. How is PCO2 related to alveolar ventilation?
The partial pressure of CO2 (PCO2) is inversely related to the alveolar ventilation and is
described by the equation:
PCO2 ¼ ðVCO2=ValveolarÞ
where VCO2 is total CO2 production and Valveolar is the alveolar ventilation (minute
ventilation less the dead space ventilation). In general, minute ventilation and PCO2 are
inversely related.
KEY POINTS: USEFUL PULMONARY EQUATIONS
1. Alveolar gas partial pressure: PAO2 ¼ FiO2 (PB PH2O) PaCO2/Q
2. Oxygen content of blood: CaO2 ¼ 1.34 [Hgb] SaO2 þ (PaO2 0.003)
3. Resistance of laminar flow through a tube: R ¼ (8 L μ)/(p r4)
4. Resistance of turbulent flow through a tube: R a r/r5
5. Calculation of shunt fraction: Qs/Qt ¼ (CiO2 CaO2)/(CiO2 CvO2)
24. What factors alter oxygen consumption?
Factors increasing oxygen consumption include hyperthermia (including malignant
hyperthermia), hypothermia with shivering, hyperthyroidism, pregnancy, sepsis, burns, pain,
and pheochromocytoma. Factors decreasing oxygen consumption include hypothermia
without shivering, hypothyroidism, neuromuscular blockade, and general anesthesia.
25. Where is the respiration center located in the brain?
The respiratory center is located bilaterally in the medulla and pons. Three major centers contribute
to respiratory regulation. The dorsal respiratory center is mainly responsible for inspiration, the
ventral respiratory center is responsible for both expiration and inspiration, and the pneumotaxic
center helps control the breathing rate and pattern. The dorsal respiratory center is the most
important. It is located within the nucleus solitarius where vagal and glossopharyngeal nerve fibers
terminate and carry signals from peripheral chemoreceptors and baroreceptors (including the
carotid and aortic bodies) and several lung receptors. A chemosensitive area also exists in the
brainstem just beneath the ventral respiratory center. This area responds to changes in
cerebrospinal fluid (CSF) pH, sending corresponding signals to the respiratory centers. Anesthetics
cause repression of the respiratory centers of the brainstem.
26. How do carbon dioxide and oxygen act to stimulate and repress breathing?
Carbon dioxide (indirectly) or hydrogen ions (directly) work on the chemosensitive area in the
brainstem. Oxygen interacts with the peripheral chemoreceptors located in the carotid and
aortic bodies. During hypercapnic and hypoxic states the brainstem is stimulated to increase
minute ventilation, whereas the opposite is true for hypocapnia and normoxia. Carbon
dioxide is by far more influential in regulating respiration than is oxygen.
27. What are the causes of hypercarbia?
n Hypoventilation: Decreasing the minute ventilation ultimately decreases alveolar
ventilation, increasing PCO2. Some common causes of hypoventilation include muscle
paralysis, inadequate mechanical ventilation, inhalational anesthetics, and opiates.
n Increased CO2 production: Although CO2 production is assumed to be constant,
there are certain situations in which metabolism and CO2 production are increased.
22 CHAPTER 2 RESPIRATORY AND PULMONARY PHYSIOLOGY
Malignant hyperthermia, fever, thyrotoxicosis, and other hypercatabolic states are
some examples.
n Iatrogenic: The anesthesiologist can administer certain drugs to increase CO2. The most
common is sodium bicarbonate, which is metabolized by the enzyme carbonic anhydrase
to form CO2. CO2 is absorbed into the bloodstream during laparoscopic procedures.
Rarely CO2-enriched gases can be administered. Carbon dioxide insufflation for
laparoscopy is a cause. Exhaustion of the CO2 absorbent in the anesthesia breathing
circuit can result in rebreathing of exhaled gases and may also result in hypercarbia.
28. What are the signs and symptoms of hypercarbia?
Hypercarbia acts as a direct vasodilator in the systemic circulation and as a direct
vasoconstrictor in the pulmonary circulation. It is also a direct cardiac depressant. Cerebral
blood flow increases in proportion to arterial CO2. An increase in catecholamines is
responsible for most of the clinical signs and symptoms of hypercarbia. Hypercarbia
causes an increase in heart rate, myocardial contractility, and respiratory rate along with a
decrease in systemic vascular resistance. Higher systolic blood pressure, wider pulse
pressure, tachycardia, greater cardiac output, higher pulmonary pressures, and tachypnea
are common clinical findings. In awake patients symptoms include headache, anxiety/
restlessness, and even hallucinations. Extreme hypercapnia produces hypoxemia as CO2
displaces O2 in alveoli.

AUTONOMIC NERVOUS SYSTEM

1. Describe the autonomic nervous system.
The autonomic nervous system (ANS) is a network of nerves and ganglia that controls involuntary
physiologic actions and maintains internal homeostasis and stress responses. The ANS
innervates structures within the cardiovascular, pulmonary, endocrine, exocrine, gastrointestinal,
genitourinary, and central nervous systems (CNS) and influences metabolism and thermal
regulation. The ANS is divided into two parts: the sympathetic (SNS) and parasympathetic (PNS)
nervous system. When stimulated, the effects of the SNS are widespread across the body. In
contrast, PNS stimulation tends to produce localized, discrete effects. The SNS and PNS generally
have opposing effects on end-organs, with either the SNS or the PNS exhibiting a dominant
tone at rest and without exogenous stimulating events (Table 1-1). In general the function of the
PNS is homeostatic, whereas stimulation of the SNS prepares the organism for some stressful
event (this is often called the fight-or-flight response).
KEY POINTS: AUTONOMIC NERVOUS SYSTEM
1. Patients should take b-blockers on the day of surgery and continue them perioperatively.
Because the receptors are up-regulated, withdrawal may precipitate hypertension,
tachycardia, and myocardial ischemia.
2. Clonidine should also be continued perioperatively because of concerns for rebound
hypertension.
3. Indirect-acting sympthomimetics (e.g., ephedrine) depend on norepinephrine release to be
effective. Norepinephrine-depleted states will not respond to ephedrine administration.
4. Under most circumstances peri-induction hypotension responds best to intravenous fluid
administration and the use of direct-acting sympathomimetics such as phenylephrine.
5. Orthostatic hypotension is common after surgery and may be caused by the use of any or all
anesthetic agents and lying supine for extended periods. It is necessary to be cognizant of this
potential problem when elevating a patient’s head after surgery or even when moving the patient
fromthe operating roomtable to a chair (e.g., procedures requiring only sedation and monitoring).
2. Review the anatomy of the sympathetic nervous system.
Preganglionic sympathetic neurons originate from the intermediolateral columns of the
thoracolumbar spinal cord. These myelinated fibers exit via the ventral root of the spinal nerve
and synapse with postganglionic fibers in paravertebral sympathetic ganglia, unpaired
prevertebral ganglia, or a terminal ganglion. Preganglionic neurons may ascend or descend the
sympathetic chain before synapsing. Preganglionic neurons stimulate nicotinic cholinergic
postganglionic neurons by releasing acetylcholine. Postganglionic adrenergic neurons synapse
at targeted end-organs and release norepinephrine (Figure 1-1).
3. Elaborate on the location and names of the sympathetic ganglia. Practically
speaking, what is the importance of knowing the name and location of these
ganglia?
Easily identifiable paravertebral ganglia are found in the cervical region (including the stellate
ganglion) and along thoracic, lumbar, and pelvic sympathetic trunks. Prevertebral ganglia
are named in relation to major branches of the aorta and include the celiac, superior and inferior
mesenteric, and renal ganglia. Terminal ganglia are located close to the organs that they serve. The
practical significance of knowing the location of some of these ganglia is that local anesthetics can
be injected in the region of these structures to ameliorate sympathetically mediated pain.
4. Describe the postganglionic adrenergic receptors of the sympathetic nervous
system and the effects of stimulating these receptors.
There are a1, a2, b1, and b2 adrenergic receptors. The A1, A2, and B2 receptors are
postsynaptic and are stimulated by the neurotransmitter norepinephrine. The A2 receptors are
presynaptic, and stimulation inhibits release of norepinephrine, reducing overall the autonomic
response. Molecular pharmacologists have further subdivided these receptors, but this is
beyond the scope of this discussion. Dopamine stimulates postganglionic dopaminergic
receptors, classified as DA1 and DA2. The response to receptor activation in different sites is
described in Table 1-2.
5. Review the anatomy and function of the parasympathetic nervous system.
Preganglionic parasympathetic neurons originate from cranial nerves III, VII, IX, and X and
sacral segments 2-4. Preganglionic parasympathetic neurons synapse with postganglionic
neurons close to the targeted end-organ, creating a more discrete physiologic effect. Both
preganglionic and postganglionic parasympathetic neurons release acetylcholine; these
cholinergic receptors are subclassified as either nicotinic or muscarinic. The response to
cholinergic stimulation is summarized in Table 1-3.
6. What are catecholamines? Which catecholamines occur naturally? Which are
synthetic?
Catecholamines are hydroxy-substituted phenylethylamines and stimulate adrenergic nerve
endings. Norepinephrine, epinephrine, and dopamine are naturally occurring catecholamines,
whereas dobutamine and isoproterenol are synthetic catecholamines.
7. Review the synthesis of dopamine, norepinephrine, and epinephrine.
The amino acid tyrosine is actively transported into the adrenergic presynaptic nerve terminal
cytoplasm, where it is converted to dopamine by two enzymatic reactions: hydroxylation of
tyrosine by tyrosine hydroxylase to dopamine and decarboxylation of dopamine by aromatic
8. How is norepinephrine metabolized?
Norepinephrine is removed from the synaptic junction by reuptake into the presynaptic nerve
terminal and metabolic breakdown. Reuptake is the most important mechanism and allows reuse
of the neurotransmitter. The enzyme monoamine oxidase (MAO) metabolizes norepinephrine
within the neuronal cytoplasm; both MAO and catecholamine O–methyltransferase (COMT)
metabolize the neurotransmitter at extraneuronal sites. The important metabolites are
3-methoxy-4-hydroxymandelic acid, metanephrine, and normetanephrine.
9. Describe the synthesis and degradation of acetylcholine.
The cholinergic neurotransmitter acetylcholine (ACh) is synthesized within presynaptic neuronal
mitochondria by esterification of acetyl coenzyme A and choline by the enzyme choline
acetyltransferase; it is stored in synaptic vesicles until release. After release, ACh is principally
metabolized by acetylcholinesterase, a membrane-bound enzyme located in the synaptic
junction. Acetylcholinesterase is also located in other nonneuronal tissues such as erythrocytes.
10. What are sympathomimetics?
Sympathomimetics are synthetic drugs with vasopressor and chronotropic effects similar to
those of catecholamines. They are commonly used in the operating room to reverse the
circulatory depressant effects of anesthetic agents by increasing blood pressure and heart rate;
they also temporize the effects of hypovolemia while fluids are administered. They are effective
during both general and regional anesthesia.
11. Review the sympathomimetics commonly used in the perioperative
environment.
Direct-acting sympathomimetics are agonists at the targeted receptor, whereas indirect-acting
sympathomimetics stimulate release of norepinephrine. Sympathomimetics may be mixed in
their actions, having both direct and indirect effects. Practically speaking, phenylephrine (direct
acting) and ephedrine (mostly indirect acting) are the sympathomimetics commonly used
perioperatively. Also, epinephrine, dopamine, and norepinephrine may be used perioperatively
and most often by infusion since their effects on blood pressure, heart rate, and myocardial
oxygen consumption can be profound. Dopamine is discussed in Chapter 15.
12. Discuss the effects of phenylephrine and review common doses of this
medication.
Phenylephrine stimulates primarily A1 receptors, resulting in increased systemic vascular
resistance and blood pressure. Larger doses stimulate A2 receptors. Reflex bradycardia may
be a response to increasing systemic vascular resistance. Usual intravenous doses of
phenylephrine range between 50 and 200 mcg. Phenylephrine may also be administered by
infusion at 10 to 20 mcg/min.
13. Discuss the effects of ephedrine and review common doses of this medication.
Give some examples of medications that contraindicate the use of ephedrine
and why.
Ephedrine produces norepinephrine release, stimulating mostly A1 and B1 receptors; the effects
resemble those of epinephrine although they are less intense. Increases in systolic blood
pressure, diastolic blood pressure, heart rate, and cardiac output are noted. Usual intravenous
doses of ephedrine are between 5 and 25 mg. Repeated doses demonstrate diminishing
response known as tachyphylaxis, possibly because of exhaustion of norepinephrine supplies or
receptor blockade. Similarly, an inadequate response to ephedrine may be the result of already
depleted norepinephrine stores. Ephedrine should not be used when the patient is taking drugs
that prevent reuptake of norepinephrine because of the risk of severe hypertension. Examples
include tricyclic antidepressants, monoamine oxidase inhibitors, and acute cocaine intoxication.
Chronic cocaine users may be catecholamine depleted and may not respond to ephedrine.
14. What are the indications for using b-adrenergic antagonists?
b-Adrenergic antagonists, commonly called b-blockers, are antagonists at b1- and
b2- receptors. b-blockers are mainstays in antihypertensive, antianginal, and antiarrhythmic
therapy. Perioperative b-blockade is essential in patients with coronary artery disease,
and atenolol has been shown to reduce death after myocardial infarction.
15. Review the mechanism of action for b1-antagonists and side effects.
b1-Blockade produces negative inotropic and chronotropic effects, decreasing cardiac
output and myocardial oxygen requirements. b1-Blockers also inhibit renin secretion and
lipolysis. Since volatile anesthetics also depress contractility, intraoperative hypotension is a risk.
b-Blockers can produce atrioventricular block. Abrupt withdrawal of these medications is not
recommended because of up-regulation of the receptors; myocardial ischemia and hypertension
may occur. b-Blockade decreases the signs of hypoglycemia; thus it must be used with caution
in insulin-dependent patients with diabetes. b-Blockers may be cardioselective, with relatively
selective B1 antagonist properties, or noncardioselective. Some b-Blockers have membranestabilizing
(antiarrhythmic effects); some have sympathomimetic effects and are the drugs of
choice in patients with left ventricular failure or bradycardia. b-Blockers interfere with the
transmembrane movement of potassium; thus potassium should be infused with caution.
Because of their benefits in ischemic heart disease and the risk of rebound, b-blockers should be
taken on the day of surgery.
16. Review the effects of b2-antagonism.
b2-Blockade produces bronchoconstriction and peripheral vasoconstriction and inhibits insulin
release and glycogenolysis. Selective b1-blockers should be used in patients with chronic
or reactive airway disease and peripheral vascular disease because of respective concerns for
bronchial or vascular constriction.
14 CHAPTER 1 AUTONOMIC NERVOUS SYSTEM
17. How might complications of b-blockade be treated intraoperatively?
Bradycardia and heart block may respond to atropine; refractory cases may require the
b2-agonism of dobutamine or isoproterenol. Interestingly, calcium chloride may also be
effective, although the mechanism is not understood. In all cases expect to use larger than
normal doses.
18. Describe the pharmacology of a-adrenergic antagonists.
a1-Blockade results in vasodilation; therefore a-blockers are used in the treatment of
hypertension. However, nonselective a-blockers may be associated with reflex tachycardia.
Thus, selective a1-blockers are primarily used as antihypertensives. Prazosin is the
prototypical selective a1-blocker, whereas phentolamine and phenoxybenzamine are examples
of nonselective a-blockers. Interestingly, labetalol, a nonselective b-blocker, also has selective
a1-blocking properties and is a potent antihypertensive.
19. Review a2-agonists and their role in anesthesia.
When stimulated, a2-receptors within the CNS decrease sympathetic output.
Subsequently, cardiac output, systemic vascular resistance, and blood pressure decrease.
Clonidine is an a2-agonist used in the management of hypertension. It also has significant
sedative qualities. It decreases the anesthetic requirements of inhaled and intravenous
anesthetics. It has also been used intrathecally in the hopes of decreasing postprocedural pain,
but unacceptable hypotension is common after intrathecal administration, limiting its usefulness.
Clonidine should be continued perioperatively because of concerns for rebound hypertension.
20. Discuss muscarinic antagonists and their properties.
Muscarinic antagonists, also known as anticholinergics, block muscarinic cholinergic
receptors, producing mydriasis and bronchodilation, increasing heart rate, and inhibiting
secretions. Centrally acting muscarinic antagonists (all nonionized, tertiary amines with the ability
to cross the blood-brain barrier) may produce delirium. Commonly used muscarinic antagonists
include atropine, scopolamine, glycopyrrolate, and ipratropium bromide. Administering
muscarinic antagonists is a must when the effect of muscle relaxants is antagonized by
acetylcholinesterase inhibitors, lest profound bradycardia, heart block, and asystole ensue.
Glycopyrrolate is a quaternary ammonium compound, cannot cross the blood-brain barrier, and
therefore lacks CNS activity. When inhaled, ipratropium bromide produces bronchodilation.
21. What is the significance of autonomic dysfunction? How might you tell if a
patient has autonomic dysfunction?
Patients with autonomic dysfunction tend to have severe hypotension intraoperatively.
Evaluation of changes in orthostatic blood pressure and heart rate is a quick and effective way
of assessing autonomic dysfunction. If the autonomic nervous system is intact, an increase in
heart rate of 15 beats/min and an increase of 10 mm Hg in diastolic blood pressure are
expected when changing position from supine to sitting. Autonomic dysfunction is suggested
whenever there is a loss of heart rate variability, whatever the circumstances. Autonomic
dysfunction includes vasomotor, bladder, bowel, and sexual dysfunction. Other signs include
blurred vision, reduced or excessive sweating, dry or excessively moist eyes and mouth, cold
or discolored extremities, incontinence or incomplete voiding, diarrhea or constipation, and
impotence. Although there are many causes, it should be noted that people with diabetes and
chronic alcoholics are patient groups well known to demonstrate autonomic dysfunction.
22. What is a pheochromocytoma, and what are its associated symptoms? How is
pheochromocytoma diagnosed?
Pheochromocytoma is a catecholamine-secreting tumor of chromaffin tissue, producing
either norepinephrine or epinephrine. Most are intra-adrenal, but some are extra-adrenal (within the
bladder wall is common), and about 10%are malignant. Signs and symptomsinclude paroxysms of
CHAPTER 1 AUTONOMIC NERVOUS SYSTEM 15
hypertension, syncope, headache, palpitations, flushing, and sweating. Pheochromocytoma is
confirmed by detecting elevated levels of plasma and urinary catecholamines and their metabolites,
including vanillylmandelic acid, normetanephrine, and metanephrine.
23. Review the preanesthetic and intraoperative management of
pheochromocytoma patients.
These patients are markedly volume depleted and at risk for severe hypertensive crises. It is
absolutely essential that before surgery, a-blockade and rehydration should first be instituted.
The a1-antagonist phenoxybenzamine is commonly administered orally. b-Blockers are
often administered once a-blockade is achieved and should never be given first because
unopposed a1-vasoconstriction results in severe, refractory hypertension. Labetalol may be the
b-blocker of choice since it also has a-blocking properties.
Intraoperatively intra-arterial monitoring is required since fluctuations in blood pressure
may be extreme. Manipulation of the tumor may result in hypertension. Intraoperative
hypertension is managed by infusing the a-blocker phentolamine or vasodilator nitroprusside.
Once the tumor is removed, hypotension is a risk, and fluid administration and administration
of the a-agonist phenylephrine may be necessary. Central venous pressure monitoring will
assist with volume management.

These secrets are 100 of the top board alerts. They summarize the concepts, principles, and most salient details of anesthesiology.

1. Patients should take prescribed b-blockers on the day of surgery and continue them
perioperatively. Because the receptors are up-regulated, withdrawal may precipitate
hypertension, tachycardia, and myocardial ischemia. Clonidine should also be continued
perioperatively because of concerns for rebound hypertension.
2. Under most circumstances peri-induction hypotension responds best to administration of
intravenous fluids and the use of direct-acting sympathomimetics such as phenylephrine.
3. To determine the etiology of hypoxemia, calculate the A-a gradient to narrow the
differential diagnosis.
4. Calculating the anion gap (Naþ [HCO

3
þ Cl ]) in the presence of a metabolic acidosis
helps narrow the differential diagnosis.
5. Estimating volume status requires gathering as much clinical information as possible
because any single variable may mislead. Always look for supporting information.
6. Rapid correction of electrolyte disturbances may be as dangerous as the underlying
electrolyte disturbance.
7. When other causes have been ruled out, persistent and refractory hypotension in trauma
or other critically ill patients may be caused by hypocalcemia or hypomagnesemia.
8. There is no set hemoglobin/hematocrit level at which transfusion is required. The decision
should be individualized to the clinical situation, taking into consideration the patient’s
health status.
9. An outpatient with a bleeding diathesis can usually be identified through history (including
medications) and physical examination. Preoperative coagulation studies in asymptomatic
patients are of little value.
10. Thorough airway examination and identification of the patient with a potentially difficult
airway are of paramount importance. The “difficult-to-ventilate, difficult-to-intubate”
scenario must be avoided if possible. An organized approach, as reflected in the American
Society of Anesthesiologists’ Difficult Airway Algorithm, is necessary and facilitates highquality
care for patients with airway management difficulties.
11. No single pulmonary function test result absolutely contraindicates surgery. Factors
such as physical examination, arterial blood gases, and coexisting medical problems also
must be considered in determining suitability for surgery.
12. Speed of onset of volatile anesthetics is increased by increasing the delivered
concentration of anesthetic, increasing the fresh gas flow, increasing alveolar ventilation,
and using nonlipid-soluble anesthetics.
13. Opioids depress the carbon dioxide–associated drive to breathe, resulting in
hypoventilation. Because of the active metabolites, patients with renal failure may
experience an exaggerated reaction to morphine.
14. Appropriate dosing of intravenous anesthetics requires considering intravascular volume
status, comorbidities, age, and medications.
15. Termination of effect of intravenous anesthetics is by redistribution, not biotransformation
and breakdown.
16. Although succinylcholine is the usual relaxant used for rapid sequence induction, agents
that chelate nondepolarizing relaxant molecule may alter this paradigm in the future.
17. Leave clinically weak patients intubated and support respirations until the patient can
demonstrate return of strength.
18. Lipid solubility, pKa, and protein binding of the local anesthetics determine their potency,
onset, and duration of action, respectively.
19. Local anesthetic-induced central nervous system toxicity manifests as excitation, followed
by seizures, and then loss of consciousness. Hypotension, conduction blockade, and
cardiac arrest are signs of local anesthetic cardiovascular toxicity.
20. There is sound scientific evidence that low-dose dopamine is ineffective for prevention and
treatment of acute renal injury and protection of the gut.
21. A preoperative visit by an informative and reassuring anesthesiologist provides useful
psychologic preparation and calms the patient’s fears and anxiety before administration of
anesthesia.
22. The risk of clinically significant aspiration pneumonitis in healthy patients having elective
surgery is very low. Routine use of pharmacologic agents to alter the volume or pH of
gastric contents is unnecessary.
23. The most important information obtained in a preanesthetic evaluation comes from a
thorough, accurate, and focused history and physical examination.
24. When compressed, some gases condense into a liquid (N2O and CO2) and some do not
(O2 and N2). These properties define the relationship between tank volume and pressure.
25. The semiclosed circuit using a circle system is the most commonly used anesthesia
circuit. Components include an inspiratory limb, expiratory limb, unidirectional valves, a
CO2 absorber, a gas reservoir bag, and a pop-off valve on the expiratory limb.
26. Every patient ventilated with an ascending bellows anesthesia ventilator receives
approximately 2.5 to 3 cm H2O of positive end-expiratory pressure (PEEP) because of the
weight of the bellows.
27. The output of traditional vaporizers depends on the proportion of fresh gas that bypasses
the vaporizing chamber compared with the proportion that passes through the vaporizing
chamber.
28. A conscientious approach to positioning is required to facilitate the surgical procedure,
prevent physiologic embarrassment, and prevent neuropathy and injury to other aspects of
the patient’s anatomy.
29. The first step in the care of the hypoxic patient fighting the ventilator is to ventilate the
patient manually with 100% oxygen.
30. Risk factors for auto-PEEP include high minute ventilation, small endotracheal tube,
chronic obstructive pulmonary disease, and asthma.
31. When determining whether an abnormal electrocardiogram (ECG) signal may be an artifact,
look to see if the native rhythm is superimposed on (marching through) the abnormal tracing.
32. A patient with new ST-segment depression or T-wave inversion may have suffered a non–
ST-elevation myocardial infarction.
33. Pulse oximetry measures arterial oxygenation using different wavelengths of light shone
through a pulsatile vascular bed. Pulse oximetry can detect hypoxemia earlier, providing
an early warning sign of potential organ damage.
34. Below a hemoglobin saturation of 90%, a small decrease in saturation corresponds to a
large drop in PaO2.
35. Except for visualization with bronchoscopy, CO2 detection is the best method of verifying
endotracheal tube location.
36. Analysis of the capnographic waveform provides supportive evidence for numerous
clinical conditions, including decreasing cardiac output; altered metabolic activity; acute
and chronic pulmonary disease; and ventilator, circuit, and endotracheal tube malfunction.
37. Trends in central venous pressures are more valuable than isolated values and should
always be evaluated in the context of the patient’s scenario.
38. Pulmonary catheterization has not been shown to improve outcome in all patient subsets.
39. The risks of central venous catheterization and pulmonary artery (PA) insertion are many
and serious, and the benefits should be identified before initiation of these procedures to
justify their use.
40. To improve accuracy in interpretation of PA catheter data, always consider the timing of
the waveforms with the ECG cycle.
41. Ipsilateral ulnar arterial catheterization should not be attempted after multiple failed
attempts at radial artery catheterization.
42. With the exception of antagonists of the renin-angiotensin system and possibly diuretics,
antihypertensive therapy should be given up to and including the day of surgery.
43. Symptoms of awareness may be very nonspecific, especially when muscle relaxants are used.
44. When a patient with structural heart disease develops a wide-complex tachycardia,
assume that the rhythm is ventricular tachycardia until proven otherwise. When a patient
develops tachycardia and becomes hemodynamically unstable, prepare for cardioversion
(unless the rhythm is clearly sinus!).
45. When a patient develops transient slowing of the sinoatrial node along with transient
atrioventricular block, consider increased vagal tone, a medication effect, or both.
46. Even mild hypothermia has a negative influence on patient outcome, increasing rates of
wound infection, delaying healing, increasing blood loss, and increasing cardiac morbidity
threefold.
47. If a patient’s exercise capacity is excellent, even in the presence of ischemic heart disease,
the chances are good that the patient will be able to tolerate the stresses of surgery. The
ability to climb two or three flights of stairs without significant symptoms (e.g., angina,
dyspnea, syncope) is usually an indication of adequate cardiac reserve.
48. Patients with decreased myocardial reserve are more sensitive to the cardiovascular
depressant effects caused by anesthetic agents, but careful administration with close
monitoring of hemodynamic responses can be accomplished with most agents.
49. For elective procedures, the most current fasting guidelines are as follows:
Clear liquids (water, clear juices) 2 hours
Nonclear liquids (Jello, breast milk) 4 hours
Light meal or snack (crackers, toast, liquid) 6 hours
Full meal (fat containing, meat) 8 hours
50. “All that wheezes is not asthma.” Also consider mechanical airway obstruction, congestive
failure, allergic reaction, pulmonary embolus, pneumothorax, aspiration, and
endobronchial intubation.
51. Patients with significant reactive airway disease require thorough preoperative preparation,
including inhaled b-agonist therapy and possibly steroids, methylxanthines, or other
agents.
52. The necessary criteria for acute lung injury/acute respiratory distress syndrome (ALI/
ARDS) include:
(1) Acute onset
(2) PaO2/FiO2 ratio of 300 for ALI
(3) PaO2/FiO2 ratio of 200 for ARDS
(4) Chest radiograph with diffuse infiltrates
(5) Pulmonary capillary wedge pressure of 18 mm Hg
53. Mechanical ventilation settings for patients with ARDS or ALI include tidal volume of at
6 to 8 ml/kg of ideal body weight while limiting plateau pressures to <30 cm H2O. PEEP
should be adjusted to prevent end-expiratory collapse. FiO2 should be adjusted to maintain
oxygen saturations between 88% and 92%.
54. Acute intraoperative increases in PA pressure may respond to optimizing oxygenation and
ventilation, correcting acid-base status, establishing normothermia, decreasing the
autonomic stress response by deepening the anesthetic, and administering vasodilator
therapy.
55. The best way to maintain renal function during surgery is to ensure an adequate
intravascular volume, maintain cardiac output, and avoid drugs known to decrease renal
perfusion.
56. Measures to acutely decrease intracranial pressure (ICP) include elevation of the head
of the bed; hyperventilation (PaCO2 25 to 30 mm Hg); diuresis (mannitol and/or
furosemide); and minimized intravenous fluid. In the setting of elevated ICP, avoid
ketamine and nitrous oxide.
57. Airway comes first in every algorithm; thus succinylcholine is the agent of choice for a
rapid-sequence induction for the full-stomach, head-injured patient, despite the
transient rise in ICP seen with succinylcholine. Succinylcholine must be avoided in
children with muscular dystrophy and should be avoided except in airway emergencies
in young males.
58. Malignant hyperthermia (MH) is an inherited disorder that presents in the perioperative
period after exposure to inhalational agents and/or succinylcholine. The disease may be
fatal if the diagnosis is delayed and dantrolene is not administered. The sine qua non of
MH is an unexplained rise in end-tidal carbon dioxide with a simultaneous increase in
minute ventilation in the setting of an unexplained tachycardia.
59. Patients with Alzheimer’s disease may become more confused and disoriented with
preoperative sedation.
60. In patients with multiple sclerosis spinal anesthesia should be used with caution and only
in situations in which the benefits of spinal anesthesia over general anesthesia are clear.
61. Patients with diabetes have a high incidence of coronary artery disease with an atypical or
silent presentation. Maintaining perfusion pressure, controlling heart rate, continuous ECG
observation, and a high index of suspicion during periods of refractory hypotension are
key considerations.
62. The inability to touch the palmar aspects of the index fingers when palms touch (the
prayer sign) can indicate a difficult oral intubation in patients with diabetes.
63. Thyroid storm may mimic MH. It is confirmed by an increased serum tetraiodothyronine
(T4) level and is treated initially with b-blockade followed by antithyroid therapy.
64. Perioperative glucocorticoid supplementation should be considered for patients receiving
exogenous steroids.
65. Obese patients may be difficult to ventilate and difficult to intubate. Backup strategies
should always be considered and readily available before airway management begins.
66. A patient with a Glasgow Coma Scale of 8 is sufficiently depressed that endotracheal
intubation is indicated.
67. The initial goal of burn resuscitation is to correct hypovolemia. Burns cause a generalized
increase in capillary permeability with loss of significant fluid and protein into interstitial tissue.
68. From about 24 hours after injury until the burn has healed, succinylcholine may cause
hyperkalemia because of proliferation of extrajunctional neuromuscular receptors. Burned
patients tend to be resistant to the effects of nondepolarizing muscle relaxants and may
need two to five times the normal dose.
69. Abrupt oxygen desaturation while transporting an intubated pediatric patient is probably
the result of main stem intubation.
70. Because children have stiff ventricles and rely on heart rate for cardiac output, maintain
heart rate at all costs by avoiding hypoxemia and administering anticholinergic agents
when appropriate.
71. Infants may be difficult to intubate because they have a more anterior larynx, relatively
large tongues, and a floppy epiglottis. The narrowest part of the larynx is below the vocal
cords at the cricoid cartilage.
72. Hyperventilation with 100% oxygen is the best first step in treating a pulmonary
hypertensive event.
73. If a child with tetralogy of Fallot has a hypercyanotic spell during induction of anesthesia,
gentle external compression of the abdominal aorta can reverse the right-to-left shunt
while pharmacologic treatments are being prepared.
74. The patient with a ventricular obstructive cardiac lesion is at high risk for perioperative
cardiac failure or arrest because of ventricular hypertrophy, ischemia, and loss of
contractile tissue.
75. Pregnant patients can pose airway management problems because of airway edema, large
breasts that make laryngoscopy difficult, full stomachs rendering them prone to aspiration,
and rapid oxygen desaturation caused by decreased functional residual capacity.
76. In preeclampsia hypertension should be treated, but blood pressure should not be
normalized. Spinal anesthesia may be preferable to general anesthesia when the
preeclamptic patient does not have an existing epidural catheter or there is insufficient
time because of nonreassuring fetal heart rate tracing.
77. Intrauterine fetal resuscitation and maternal airway management are of overriding
importance in patients with eclamptic seizures.
78. Basal function of most organ systems is relatively unchanged by the aging process per se,
but the functional reserve and ability to compensate for physiologic stress are reduced.
79. In general, anesthetic requirements are decreased in geriatric patients. There is an
increased potential for a wide variety of postoperative complications in the elderly, and
postoperative cognitive dysfunction is arguably the most common.
80. Anesthesiologists increasingly are asked to administer anesthesia in nontraditional
settings. Regardless of where an anesthetic is administered, the same standards apply for
safety, monitors, equipment, and personnel.
81. O-negative blood is the universal donor for packed red blood cells; for plasma it is AB positive.
82. If a patient is pacemaker dependent, the interference by electrocautery may be interpreted
by the device as intrinsic cardiac activity, leading to profound inhibition of pacing and
possible asystole. Devices should be programmed to the asynchronous mode before
surgery.
83. Pacemaker-mediated tachycardia is an endless-loop tachycardia caused by retrograde
atrial activation up the conduction system, with subsequent tracking of this atrial signal
and then pacing in the ventricle. It can be terminated by application of a magnet that
prevents tracking.
84. Loss of afferent sensory and motor stimulation renders a patient sensitive to sedative
medications secondary to deafferentiation. For the same reason neuraxial anesthesia
decreases the minimum alveolar concentration of volatile anesthetics.
85. Patients with sympathectomies from regional anesthesia require aggressive resuscitation,
perhaps with unusually large doses of pressors, to reestablish myocardial perfusion after
cardiac arrest.
86. Although patients with end-stage liver disease have a hyperdynamic circulation characterized
by increased cardiac index and decreased systemic vascular resistance, impaired myocardial
function, coronary artery disease, and pulmonary hypertension are common.
87. Patients with liver disease commonly have an increased volume of distribution,
necessitating an increase in initial dose requirements. However, because the drug
metabolism may be reduced, smaller doses are subsequently administered at longer
intervals.
88. There is no best anesthetic technique during cardiopulmonary bypass. Patients with
decreased ejection fraction will not tolerate propofol infusions or volatile anesthesia as
well as patients with preserved stroke volume and will probably require an opioid-based
technique.
89. Always reassess optimal positioning of any lung-isolation device after repositioning the
patient. A malpositioned tube is suggested by acute increases in ventilatory pressures and
decreases in oxygen saturation.
90. Methods to improve oxygenation during one-lung ventilation include increasing FiO2,
adding PEEP to the dependent lung, adding continuous positive airway pressure to the
nondependent lung, adjusting tidal volumes, and clamping the blood supply to the
nonventilated lung.
91. To decrease airway pressures, always use the largest double-lumen endotracheal tube
available.
92. If ICP is high, as evidenced by profound changes in mental status or radiologic evidence of
cerebral swelling, avoid volatile anesthetics and opt instead for a total intravenous
anesthetic technique.
93. If PaCO2 significantly increases after 30 minutes of pneumoperitoneum, search for another
cause of hypercapnia such as capnothorax, subcutaneous PaCO2, CO2 embolism, or
endobronchial intubation.
94. Pulmonary arterial occlusion pressure is an unreliable indicator of cardiac filling pressures
during pneumoperitoneum.
95. Postoperative nausea and vomiting are common after laparoscopic surgery; they should
be anticipated and treated prophylactically.
96. Methohexital should be considered the drug of choice for the induction of anesthesia for
electroconvulsive therapy (ECT). ECT causes pronounced sympathetic activity, which may
result in myocardial ischemia or even infarction in patients with coronary artery disease.
97. To perform ECT safely it is necessary to complete a preoperative history and physical
examination, use standard monitors, have readily available equipment and medications
appropriate for full cardiopulmonary resuscitation, use an induction agent (e.g.,
methohexital) and muscle relaxant (e.g., succinylcholine), and have a b-blocker readily
available (e.g., esmolol).
98. Doses of morphine differ by a factor of 10 between intravenous, epidural, and intrathecal
routes.
99. Chronic pain is best treated by using multiple therapeutic modalities, including physical
therapy, psychologic support, pharmacologic management, and rational use of more
invasive procedures such as nerve blocks and implantable technologies.
100. Neuropathic pain is usually less responsive to opioids than pain originating from
nociceptors.

Complications of Local Anesthesia

Introduction: Local anesthetic complications can be divided into two areas. There are local complications and systemic complications. Local complications are the result of the mechanics of the injection or the properties of the anesthetic drug on the local environment. Systemic complications are those general complications occurring as a result of the drug used or a local problem that can lead to systemic sequela.

Required reading: Handbook of Local Anesthesia, Fourth Edition, Stanley F. Malamed, Mosby Publishing Company. Chapters, 17 and 18. Pages 246-286. Chapter 20. Pages 303-310.  

I. Local complications 

A. Needle Breakage

1. Causes- needle size, smaller more likely, prior bending of needle unexpected patient movement, defective needles

2. Problems, if retrievable, if not retrievable easily

3. Prevention - larger gauge for deep penetrating injections, longer needles, do not insert to hub, do not bend needle, do not redirect needle when in deep tissue.

4. Management - calm, no panic, inform patient, no movement patient, keep mouth open. Use hemostat to retrieve if possible. If not visible refer to competent surgeon. If superficial and easily identified surgeon removes. May have to leave in if deep or difficult to find. However it is better to have it removed if possible. Possible litigation highly likely. 

B.  Pain on Injection

1. Causes - Careless injection technique, dull needle, rapid injection, barbed needles. 

2. Problems - anxiety increase, unexpected movement and its sequela.

3. Prevention - proper injection technique, sharp needles, topical, sterile LA soln., slow injection, room temperature anesthetic soln.

4. Management - prevention is management.

C. Burning on Injection

1. Causes - ph LA Soln, rapid injection, contamination cartridge, rapid injections, warmed soln.

2. Problem - none if due to ph, (usually), if due to contamination tissue damage, trismus, edema, parasthesia.

3 Prevention - prevention, slow injection, (ideal, 1ml/min, recommended not more than 1.8ml/min)

4. Management - specific problems that arise are managed.

D.  Persistent Anesthesia or Parasthesia - Anesthesia lasts for longer than expected. Some patients are hyperreactors, longer anesthesia. However some anesthesia lasts week, months, years. Longer lasting increases problems. Parasthesia, anesthesia may not be preventable. Parasthesia results in many malpractice suits.

1. Causes - alcohol contamination LA, solutions. Sterilizing solution contamination LA. Trauma to nerve with needle. Inserting a needle into a foramen increases risk of nerve trauma. Hemorrhage in and around neural sheath secondary to trauma.  

2. Problem - patient can injure anesthetized area. Bite, burn, chemical injury. Lingual nerve damage effect taste. Can get hyperesthesia or dysesthesia. Prilocaine apparently involved in paresthesia more often than other LA agents.

3. Prevention - observe protocol for handling and care of LA cartridges. Parasthesia can still occur.

4. Management - most parasthesias resolve in about 8 weeks without treatment. Sever damage may lead to permanent anesthesia, rare. Most paresthesia is minimal. In general dentistry most parasthesias involve tongue. Reassure patient, you speak directly to patient. Explain paresthesia to patient and usual course. Examine patient. Chart location and depth. Record incident on record. Some waiting indicated. Sensory deficit of three months get consultation with oral and maxillofacial surgeon and or neurologist. Avoid dental injections in same area of injury to nerve. Steroids may be indicated at time of or shortly after injury. If you are aware of the nerve injury at the time of surgery steroids also may be indicated.

E.  Trismus - Prolonged spasm of the jaw muscles. Restriction of opening. Can be used to indicate any limitation of movement. Can be chronic and difficult to manage.

1. Cause - Most common cause from dental injections is the trauma to blood vessels or muscles in the infratemporal fossa. Contaminated cartridges, with alcohol or sterilizing solution cause tissue damage. Intramuscular injections LA. Hemorrhage in area. Infection post injection.     Multiple injections in same area. Barbed needles. Barbed needles. Large amounts of LA solution in same area.

2. Problems - limitation usually minor and transient. Can become sever and chronic. Can require extensive therapy and or surgery. 

3. Prevention - sharp needles, care of cartridges, aseptic technique, atraumatic injection, know anatomy, avoid multiple injections same area, use minimum effective volume.

4. Management - Pain and trismus usually occurs 1-6 days post injection. See patient. Rx. Analgesics, heat, warm rinses and muscle relaxants if indicated. Initiate physical therapy. Opening and closing. Use of tongue blades to stretch. Gum chewing. Antibiotics if indicated. If severe and no response within 2-3 days no antibiotics, and 5days with antibiotics refer to oral and maxillofacial surgeon. Severe dysfunction can require surgery.

 F.  Hematoma

1. Causes - puncture artery or vein.
2. Problem - Swelling, discoloration, bruise, trismus, pain and infection rare
3. Prevention - Knowledge of the anatomy. Certain blocks more likely. PSA most. Inf. Alveolar, mental. Modify technique for smaller adults. Reduce number of punctures. Do not probe with needle.

4. Management - direct pressure immediate. Two minutes. Inf. Alveolar against medial portion mandible. Infra orbital, skin over foramen. PSA side of face. Ice to face. Intraoral pressure at site of injection. Usually can be large hematoma. Record hematoma=s in patients chart. Inform patient of sequeli. No heat four to six hours post injection. Can use ice or cold rinses. Usually resolves 7-10 days. 

G.  Infection 

1. Causes - Needle contamination. Usually not from local flora. Usually from improper handling of the injection set up. Injecting through a an infected area to non infected

2. Problem - Low-grade infection in deeper tissue. Trismus possible. Must recognize infection.

3. Prevention - Disposable needles. Handle cartridges well. Store well. Do not contaminate cartridge solution. Cap needle. Do not touch to non sterile surface. Wipe diaphragm with sterile disposable alcohol let dry.

4. Management - Difficult to diagnose. Trismus may be sign. Treat trismus. No response in three days then place on antibiotic. Use penicillin or appropriate antibiotic if allergic to penicillin for at least seven days. Record progress and if no response refer to Oral and Maxillofacial surgeon or other specialist if indicated.

H.  Edema - Swelling of the tissue. Sign of other disorder.

1. Causes -Trauma, infection, allergy and hemorrhage.

2. Problem - swelling usually not a problem. Some pain discomfort. Angioneurotic edema may be life threatening. Can compromise airway.

3. Prevention - handling injection equipment. Atraumatic injection. Complete medical evaluation patient.

 

4. Management - traumatic may be small and self-resolving. Bleeding requires pressure, ice. Infection usually requires antibiotics or other treatment. Allergy induced edema can be life threatening. Airway may be compromised. If unconscious provide basic life support, call 911, secure airway if possible. Epinephrine, Corticosteroid, Antihistamine, possible cricothyrotomy. Later evaluate cause. 

I.  Sloughing of Tissue

1. Causes - Epithelial Desquamation, sterile abscess.

2. Problem - Pain

3. Prevention - Use topical anesthetic as directed. Do not use high concentration vasoconstrictor. 

4. Management - Symptomatic for pain. Systemic analgesics, topical orabase.

J. Soft Tissue Injury - Self inflicted injury.

1. Causes - self inflicted, children, mentally or physically disabled. Soft tissue anesthesia.

2. Problem - swelling, pain. Infection rare.

3. Prevention - Select LA for duration of procedure. Instruct parents or patient. Sticker warning on children.

4. Management - Analgesics, antibiotics,   lubricants of needed.

 k. Facial Nerve Paralysis - Paralysis of branches of the seventh nerve.

1. Causes - Infraorbital block, Maxillary canine infiltration, Inferior alveolar injection into parotid gland.
2. Problems – Pt. Anxiety, unable to close eye. Unilateral facial paralysis, (secondary to inferior alveolar in parotid gland.
3. Prevention – Know anatomy. With Inferior alveolar touch bone. If using Vazarani- Akinosi know landmarks, with gow gates know landmarks.

4. Management – Paralysis shows up quickly. Reassure patient. Explain. Eye patch. Instruct in eye care. Lubricate eye. Record incident. Stop procedure.

L. Post Anesthetic Intraoral Lesions – Usually several days after injections in area of injection.

1. Causes – recurrent aphthous ulcers or herpes simplex. Trauma needles, swab, and may activate latent forms.
2. Problem – pain, sensitivity
3. Prevention – not known. Can treat prodromel syndrome with antiviral agents. Usually runs its course.
4. Management – Reassure patient. Not bacterial. Will run course. Follow patient. Can occur again