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6. Shock in surgery
6.1 General remarks
1. Excessive bleeding is a leading cause of morbidity and mortality. Traumatic injury and its
sequelae are the principal causes of death in patients aged 1 to 44 years in the US. In a study
assessing the epidemiology of trauma deaths (Baker et al.) 53% of trauma victims died at the
scene, 7.5% in the emergency room, and the remaining 39.5% in the hospital. The most
common cause of death was central nervous system injury, representing 50% of the
population studied. Hemorrhage was responsible for 31% of deaths, whereas 18% died due to
sepsis.
2. Shock ≠ hypotension. Hypotension is not an early sign of shock. Not all hypotension is
shock and not all shock has hypotension.
3. Shock = ”a momentary pause in the act of death” (John C. Warren, 1895). To catch early
you must have a high index of suspicion!
4. Shock is a medical condition, and not a diagnosis. Often classified by the cause of the
syndrome: hypovolemic (e.g. hemorrhagic), cardiogenic, distributive (e.g. septic, neurogenic),
obstructive (e.g. cardiac tamponade). However, there are more than 100 „shock states”- these
types are not mutually exclusive categories, two or more types are often combined:
hypovolemia may occur with septic shock, elements of cardiogenic shock may occur in other
types of shock, etc.
5. Regardless of the classification, the underlying defect is always inadequate tissue perfusion.
Irrespective of cause, the hypoperfusion-induced imbalance between the delivery of and
requirements for oxygen and substrate leads to cellular dysfunction. „Shock is not something
that is broke that you fix and are done. It is an evolving process that is a symptom of
something else going wrong with the patient, that left untreated can result in death” (Source:
Harrison's Principles of Internal Medicine, 16th Edition 2005. P10, S2: Shock and Cardiac
Arrest)
6.2. Definition of circulatory shock
A state in which there is inadequate tissue perfusion to meet metabolic demands. The essential
pathogenetic factor in all types of shock is a significant discrepancy between oxygen uptake
and oxygen demand. Tissues in widespread areas of the body are being damaged by nutritive
insufficiency resulting either from an insufficient oxygen delivery to cells / inability of the
cells to utilize oxygen.
VO2
= O2 consumption
Flux O2
= O2 transport = DO2 (mL O2/min) = CaO2 (ml O2/l blood) x CO (l/min)
(cardiac output x arterial O2 content)
Ca O2- Cv O2
Ex O2 = extraction ratio = ----------------------Ca O2
VO2 = Flux O2 x Ex O2
6.3. The essential patterns of circulatory shock
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6.4. The mean arterial pressure
Mean arterial pressure (MAP) affects oxygenation of any organ or tissue. Average pressure
within the cardiovascular system through one cardiac cycle is calculated by: MAP = systolic +
(2) diastolic divided by 3. Factors influencing MAP:
Total blood volume (direct relationship)
Cardiac output (direct relationship)
Size of the vascular bed (inverse relationship)
6.5. Bleeding and the time factor
With small volume and pressure declines, compensations can restore pressure. If losses are
large, there is no recovery. Outcomes of same volume lost over different periods: slow losses
allow compensations to take effect. Rapid loss of same volume is fatal. Rapidity of diagnosis
is key!
6.6. Main compensatory mechanism in low flow shock states
Volume loss and declining blood pressure will lead to vasoconstriction. The key to peripheral
vascular resistance is the arteriolo-capillary junction. Immediate consequences are circulatory
redistribution, TPR increase, ejection fraction increase, and increase in venous return.
6.7. Compensatory mechanisms after blood loss
1. Baroreceptor reflex: responds to small changes in vascular tone/pressure. Leads to
decreased vagal tone, which increases HR, decreases coronary resistance (improves
myocardial oxygen supply). Sympathetic tone is increased, which causes venoconstriction,
constriction of blood reservoirs (increasing circulating blood volume), decreased perfusion in
skin and skeletal muscle.
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2. Chemoreceptors are sensitive to oxygen and carbon dioxide and sense hypoxia (due to
inadequate blood flow in peripheral tissues). Prominent chemoreceptors are the carotid and
aortic bodies. Reflexes that regulate blood pressure are integrated in the medulla. Further
vasoconstriction and respiratory stimulation - improves venous return (pump model), also
helps compensate for acidosis.
3. Endogenous vasoconstrictors: adrenal medulla hormones – norepinephrine and epinephrine
cause vasoconstriction and increased cardiac output. Vasopressin (ADH) released from
posterior pituitary causes intense vasoconstriction in cases of extremely low MAP. Renin
(from decreased renal perfusion) leads to angiotensinogen and angiotensin II production.
Endothelium-derived factors – endothelin-1 and prostaglandin-derived growth factor (PDGF)
are both potent vasoconstrictors
4. Reabsorption of tissue fluids: “one great consequence of blood loss is the intense
vasoconstriction, the shrinkage of the capacity of the vascular bed to accommodate the
decreased blood volume...adjustments for blood loss take place...the entry of fluid into the
blood vessels in a compensatory attempt. The greatest extravascular store of readily available
fluid in the body is...in the extracellular space.” (Source: Beecher et al: Recent Advances in
Surgery I. The Internal State of the Severely Wounded Man on Entry to the Most Forward
Hospital. Surgery 22:672-711, 1947).
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5. Renal conservation of water: aldosterone release stimulated by vasopressin causes sodium
reabsorption in distal tubules. Water follows the sodium.
6. Cerebral ischemia (when cerebral perfusion pressure < 40 mmHg) activates
sympathoadrenal system, increases catecholamine release from both adrenal gland and
sympathetic nerves (can also get vagal stimulation which is counterproductive).
6.8. Decompensatory mechanisms after blood loss
1. Cardiac failure has many potential etiologies (i.e. actual etiology is controversial).
Myocardial strength may decrease from ischemia secondary to a reduction of circulating
RBCs, lower oxygen saturation, decreased coronary perfusion secondary to hypotension
(especially diastolic hypotension).
2. Hypoperfusion => anaerobic metabolism => lactic acidosis. Depressant of myocardial
function, decreased response to catecholamines both in myocardium and peripheral
vasculature.
3. Central nervous system depression: due to opioid release (enkephalins, beta-endorphin).
Naloxone has been used as treatment in shock, with some success.
4. Disseminated intravascular coagulation (DIC): abnormalities of clotting system develop as
a result of attempt to control hemorrhage but also dilution/loss of clotting factors.
Gastrointestinal hemorrhage is seen as complication of acute hemorrhage, hours after the
initial event
5. Reticuloendothelial system dysfunction: lose antibacterial function can get endotoxin
release from native bacteria, aggravates already compromised situation.
6. Microcirculatory collapse.
6.9. Microcirculation
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Anatomy: interwoven networks of capillaries with vascular shunts, metarteriole –
thoroughfare channel connecting an arteriole directly with a postcapillary venule. True
capillaries: 10 – 100/capillary bed, branch off the metarteriole and return to the thoroughfare
channel at the distal end of the bed. Precapillary sphincters: cuff of smooth muscle surrounds
each true capillary.
6.9.1. Microcirculatory dysfunction
Decreasing flow /haematocrit in the arteriole => increasing flow in thoroughfare channels.
Consequences: train flow, flow stops without cellular blockade, endothelial cell - leukocyte
interactions in postcapillary venules, erythrocyte diapedesis, leukocyte extravasation,
leukocyte blockage.
6.10. Stages of hemorrhagic shock
1. Compensated shock: entails some decreased tissue perfusion, but the body's compensatory
responses are sufficient to overcome the decrease in available fluid.
2. Decompensated shock: blood moves to more vital organs. Precapillary sphincters relax due
to shock-related stimuli. Postcapillary sphincters resist local effects and remain closed =>
pooling /capillary stasis, capillary engorgement. Increasing hypoxemia and acidosis lead to
opening of additional capillaries, the vascular space expands greatly. Even a normal blood
volume may be inadequate to fill the container, but the capillary and venule capacity may
become great enough to reduce the volume of available blood for the vena cava. Decreased
venous return => fall in CO. Viscera (lung, liver, kidneys, gastrointestinal mucosa): congested
due to stagnant blood flow. Respiratory system: attempts to compensate for the acidosis by
increasing respiratory rate and producing a partially compensated metabolic acidosis. Clotting
mechanisms: hypercoagulability (DIC). Decompensated shock progresses to irreversible
shock if fluid resuscitation is inadequate or delayed.
3. Irreversible shock: multiple system / organ damage, even with treatment, death is the result.
Occurs when the body is no longer able to maintain systolic pressure. Both the systolic and
diastolic pressure begin to drop. Pulse pressure may be narrowed to such an extent that it is
not detectable with a blood pressure cuff. The loss of arterial pressure causes damage from
which ultimate recovery is not possible despite temporary restoration of MAP. Signs:
bradycardia, serious dysrhythmias, severe hypotension, evidence of multiple organ failure,
pale, cold, and clammy skin, noticeably delayed/no capillary refill, cardiopulmonary collapse.
6.11. Complications of hemorrhagic shock
Fever, brain death
Adult respiratory distress syndrome (ARDS)
Centrilobular hemorrhagic necrosis of the liver
Acute tubular necrosis of the kidney
Superficial hemorrhagic necrosis of intestine
Focal myocardial necrosis
Congestion and hypersplenia of spleen
Stress ulcers of stomach
Vasodilation and splanchnic pooling
6.12. Treatment
Evaluation: internal or external hemorrhage; underlying cardiac problems; determine the
amount of blood loss; how long has been bleeding?
Level of consciousness (“Report and Record”): alert - verbal response to stimuli - pain
response to stimuli - unresponsive to any stimuli.
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Goals: to increase tissue perfusion and oxygenation status, and to treat the underlying cause.
First steps: positioning, ABCD approach, keeping the patient at normal temperature, prevent
hypothermia. On-going assessment - every 10-15 min.
1) Airway: needs will vary depending on etiology of shock, from no intervention to
aggressive intervention.
2) Breathing: patients need respiratory support (intubation or other respiratory support) and
monitoring. Exogenous O2 helps with oxygen delivery even though saturation may be normal
– it helps to compensate for a profound metabolic acidosis.
3) Circulation: replacement therapy, volume should be given. Crystalloids: normal saline is
the solution of first choice because it is ubiquitously available in health care settings
(including ambulances) and carries minimal risk. Amount is 3:1 (therapy: loss). Initial volume
is always at least 20 ml/kg. In most cases of early shock it will take still more volume than
this to correct deficits. Colloids are given in 1:1 ratio (human albumin, hydroxyethyl starch
(HES + 0.9% NaCl, or RL), hypertonic saline-dextran combinations). Transfusion - 2U blood
or RBC, if instability persists after 2000 mL crystalloid. Active bleeding: several U blood.
Important items:
- Warming!
- Take blood samples before transfusion!
4. Definitive therapy /Drugs: goals are to increase preload, increase contractility and decrease
afterload. Correction of acidosis: Na-bicarbonate is given if the deficit > 6 mEq/l. Useful
formula: 0.3 x kgbw x base deficit = mEq NaHCO3 will compensate for half of the loss. It
should be given slowly in 1-2 mEq/kg bolus - 10-20 mEq/kg could be needed which means
large Na+ load and hyperosmolarity. Background: pH < 7.25 will interfere with the effects of
catecholamines = inotropic resistant hypotension evolves.
Caveat: „although this is a time-honored concept, recent data do not find evidence of this
phenomenon. Metabolic acidosis is a sign of underlying lack of adequate oxygen delivery or
consumption and should be treated with more aggressive resuscitation, not exogenous
bicarbonate.. “ (Source: John P. Pryor, Hemorrhagic Shock, 2004)
5. Treatment with pressors
Alpha
Peripheral
Beta 1
Cardiac
Beta 2
Peripheral
Norepinephrine
alpha and beta, more alpha
++++
++++
0
Epinephrine
beta and alpha, stronger beta
++++
++++
++
Dopamine
++++
++++
++
Isoproterenol
0
++++
++++
Dobutamine
beta-1 alone
+/0
++++
+
Source: NEJM, 300:18, 1979
Consider the main effects as follows:
- β effects: increase inotropy and chronotropy - increasing cardiac output (beta-1) also some
pulmonary and peripheral vasodilation (beta-2)
- α effects: increase systemic vascular resistance - maintaining blood pressure
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- vasodilators: decrease systemic vascular resistance - decrease afterload, potentially
improving cardiac function, but also dramatically reducing MAP in hypovolemic patient.
β1 myocardium:  contractility
β2 arterioles: vasodilation
β1 SA node:  chronotropy
β2 lungs: bronchodilation
α peripheral: vasoconstriction
Dopamine: dopaminergic at low doses, beta at medium to high and alpha at high doses:
renal (2-4 µg/kg/min) dose: increase in mesenteric blood flow;
β (5-10 µg/kg/min) dose: modest positive ionotrope;
α (10-20 µg/kg/min) dose: vasoconstriction.
6. Electrolytes
Na+ can be markedly abnormal as a result of the underlying disease (hypo/hypernatremic
dehydration); can get elevated during process of correcting base deficit. Goal should be to
normalize Na+ - slowly!
K+ can be elevated to the point of cardiac dysrhythmias, as correction of acidosis occurs K+
can be driven back into cells developing severe hypokalemia in some cases.
Ca++ can be chelated in treatment of base deficit and dramatically decrease, leading to
problems from seizures, hypotension and myocardial dysfunction
Glucose: as part of response to compensatory mechanisms (epinephrine and corticosteroids)
hyperglycemia is a common occurrence in stressed children. This can cause problems from
osmotic diuresis and glucose intolerance. Care should be made not to overload the glucose
management system in the body (i.e. no dextrose in flush solutions)
Blood gases: it is important to maintain good DO2 to help minimize anaerobic metabolism
and worsening of acidosis. Venous blood gases are also of benefit since mixed venous O2
saturation is a measurement of tissue perfusion and CO.
7. Monitoring
CVP
Hemodynamics: MAP and ECG
Coagulation status: DIC is a common complication even early in shock.
Urine output: representative of organ perfusion, improving urine output can be a sign of
improving volume status, while worsening output suggests the need for more aggressive
therapy.
Neurologic status: indicative for brain perfusion.
6.13. Reversal of cardiovascular instability
- Clinical history and observations – Pulse, blood pressure, skin turgor, stable MAP
- Slowing HR
- Increased level of consciousness, decreased anxiety
- Improved capillary refill, improved color of mucous membranes
- Warming of the extremities
- Urinary output > 30 ml/h
- CVP or pulmonary capillary wedge pressure
- Response of CVP to fluid challenge: a fluid challenge should be regarded as a 200-250 ml
bolus of colloid. This should be administered as quickly as possible. A response in the CVP or
urine output should be seen within minutes. The size and duration of the CVP response rather
the actual values recorded is more important.
6.14. Variations in physiological responses to hemorrhagic shock
Age and relative health
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General physical condition
Preexisting diseases
Ability to activate compensatory mechanisms
Older adults are less able to compensate (develop hypotension early)
Children compensate longer and deteriorate faster
Medications may interfere with compensatory mechanisms
6.15. Medical – legal pitfalls
Non-recognized occult bleeding.
Hypotension after head trauma (hypotension + other causes!).
Omission of rectal finger exam.
Undiagnosed bleeding source.
Inadequate resuscitation (immediate, correct, sustained therapy)
6.16. Crystalloid versus colloid resuscitation
Several randomized controlled trials of crystalloid vs. colloid resuscitation published. None
has shown either type of fluid to be associated with a reduction in mortality. No single type of
colloid has been shown to be superior; albumin solution may be associated with slight
increase in mortality. Colloids can more rapidly correct hypovolaemia, and also maintain
intravascular oncotic pressure. Crystalloids require large volume but are equally effective,
cheaper and have fewer adverse side effects. Hypertonic solutions are subjected to recent
intensive investigation, can resuscitate patient rapidly with a reduced volume of fluid and may
reduce cerebral edema in patients with severe head injuries
6.17. Oxygen carrying agents
Currently being extensively investigated in clinical trials. Potential advantages over blood
include: free from potential viral contamination, universal ABO compatibility, oxygencarrying capacity is similar to blood. Agents being studied include: perflurocarbons, human
haemoglobin solutions, polymerised bovine hemoglobin.
6.18. Intraosseous infusion
Venous access can be difficult in the hypovolaemic child. If difficulty experienced then
intraosseous route can be used as an alternative. Medullary canal in a child has a good blood
supply, drugs and fluids are absorbed into the venous sinusoids of red marrow. Less effective
in older children, systemic drug levels are similar to those achieved via the intravenous route.
Technique is generally safe with few complications. Indications: major trauma, extensive
burns, cardiopulmonary arrest, septic shock. Contraindications: ipsilateral lower limb fracture,
vascular injury. Technique: specially designed needles. Short shaft allows accurate placement
within the medullary canal, handle allows controlled pressure during introduction. Usually
inserted into anterio-medial border of tibia, 3 cm below tibial tubercle, correct placement
checked by aspiration of bone marrow. Both fluids and drugs can be administered, fluid often
needs to be administered under pressure. Once venous access achieved the intraosseous
needle can be removed.
6.19. Endotracheal intubation
Definition
Introducing a plastic or rubber tube through the mouth or nose into the trachea to secure
open airways in a sedated or anesthetized patient. In some situations this procedure can be
performed in conscious state (awake intubation). If the endotracheal tube is no longer
required, it can be removed (extubation).
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6.19.1. Securing open airways
Securing open airways is one of the most important tasks of anesthesiologists during surgery.
This can be performed by tilting the patient’s head backward to elevate the tongue from the
posterior pharynx (extratracheal method) with using oropharyngeal or nasopharyngeal tubes
or laryngeal masks. However, endotracheal intubation is the most reliable method of securing
the airways during surgery or emergency situations, accidents
Advantages of endotracheal intubation
1. The anatomic dead space can be decreased by 50%. Alveolar ventilation will be increased
even in high risk surgical patients.
2. Positive pressure ventilation can be used, and the ventilated air and anesthetic gas mixture
can only reach the lungs (instead of stomach).
3. Vomiting and aspiration can be avoided.
4. Suctioning of fluids from the lungs can be performed.
5. Atelectasis can be eliminated by using artificial ventilation.
6. Re-positioning of the patient does not affect ventilation.
7. Different drugs can be given intratracheally.
6.19.2. Equipment
- Oxygen supply
- Face mask for pharyngeal tubes, cuffed or simple endotracheal tubes.
- Laryngoscopes with blades in different size and type.
- Syringes to inflate the cuff, Péan forceps to clamp the duct of the balloon.
- Magill forceps (introducer).
- Medications.
- Suction apparatus to remove fluids („bronchial toilette”).
6.19.3. Technique of intubation
Intubation can be performed under direct visualization with the help of a laryngoscope
(direct laryngoscopy). The procedure can be done through the mouth or nose in narcosis or
relaxed state, or deep unconsciousness, or state of clinical death.
1. Prepare first the required equipments, tools, drugs on the table next to the patient. Check
them consecutively:
- Ruben-balloon with valve and mask;
- suction pump with suction catheter;
- laryngoscope;
- endotracheal tubes;
- tube adaptors;
- syringe for inflation of cuff;
- Péan for clamping the duct of cuff;
- bite block (Guedel-tube or 10x5 gauze strip);
- tape for fixing the tube.
If the patient is apnoic or the breathing is insufficient, ventilation through the mask must be
applied until the tools are prepared.
2. The patient should lie in a supine position, the head is toward the person performing the
procedure.
3. Apply general or local anesthesia in the patient’s pharynx or larynx. .It is also useful to
apply surface anesthesia, because anesthesia of larynx and trachea decreases reflex
excitability. In local anesthesia, excitation of vagus is minimal, heart rhythm disorder is
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rarely occurred, patients tolerate the tube well, and laryngospasm following extubation is
rare.
Larynx analgesia is achieved by applying 10% Lidocain spray (2 or 3 spurts; 1 spurt is
equal to 4.8 mg). During spontaneous ventilation, after inserting the blade of laryngoscope
application of Lidocain spray together with inspiration results in sufficient analgesia at the
upper part of trachea. If the distal end of tube is also sprayed with Lidocain before
intubation, the patient will also tolerate the tube after recovering consciousness.
4. Deliver oxygen with a face mask for at least 3 minutes. If intubation fails in short time (no
more than one minute) in the non-breathing patient, apply ventilation through the mask, and
intubation should be performed again only in the well-oxygenated patient.
5. Place the patient’s head in proper position, remove pillow from under the shoulder. The
Jackson position makes exploration of the larynx easy. In adults the narrowest part of the
airways is the glottis (subglottis in children). In supine position there is an open obtuse angle
between the oral and pharyngeal axis. There are two positions for the alignment of the two
axes and the easier passage of the endotracheal tube.
5.1. Jackson position: in most cases the patient is laid in supine position without a pillow.
The palm is placed on the patient’s forehead and pushes it down, so the head is tilted
backward at the atlanto-occipital joint (the cervical spine is also turned backward). The oral
axis approaches the pharyngeal so the glottis can be illuminated easily with the blade of
laryngoscope.
5.2. Modified Jackson position: in supine position (short-neck, fat patient, torticollis, etc.) a
10-15 cm pillow is placed under the patient’s nape, and the head will be tilted so that the
mouth will open. The oral axis coincides with the pharyngeal one, and the glottis can be
seen with the laryngoscope underneath.
6. Paralyze the patient with depolarizing (succinylcholine) or non-depolarizing agents.
7. Stand behind the patient laid in Jackson position, grasp the laryngoscope in the left hand
and insert the curved blade into the mouth along the median of tongue. (If the mouth can be
opened only a little bit, or the tongue is too large, push the tongue to the left to create larger
place for intubation. In most cases it is unnecessary. Sometimes stylets and rarely bronchofiberoscope are needed.)
When the muscles are relaxed, explore the pharyngeal-laryngeal area with the laryngoscope in
the left hand, and insert the tube with the right hand. Approaching the base of the tongue the
floppy epiglottis can be seen. Then, push the blade 1 or 2 cm forward while lifting the handle
of the laryngoscope. (Do perform intubation with attention to the teeth: do not lean against the
upper teeth and do not tilt the handle toward the teeth!) The end of the blade is between the
base of tongue and the epiglottis, in the plica glossoepiglottica. Lifting the base of the tongue
can also move the epiglottis (due to the lig. hypoepiglotticum between the corpus ossis
hyoidis and the cartilago epiglottidis) and the triangular glottis with its peak upward can also
be emerged. If the epiglottis and the front of trachea can not be seen, the assistant should press
down the base of thyroid cartilage and the cricoid cartilage (Sellick maneuver). The
endotracheal tube in the right hand should be inserted from the right side of the mouth in the
glottis, and then into the trachea. The tube is pushed 4 or 5 cm forward, until the cuff will
disappeared in the glottis.
Pay attention not to damage soft tissues with the blade of laryngoscope, not to reach the
epiglottis, and not to force the tube into the narrow glottis. Do not turn the laryngoscope but
lift it up for better visualization. Hold the tongue so not to be in the way of field of vision.
8. Depth of intubation is indicated on the tube. It can be read on the sign of tube. The distance
of tracheal bifurcation from the front teeth is approx. 23 and 27 cm in women and men,
respectively. For the appropriate oxygenation of the lung, the end of the tube has to be 1-3 cm
above bifurcation.
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Following the proper positioning the tube, cuff must be inflated and control balloon is closed,
then. In newer models, (i.e.: low-pressure cuffs) the balloon is closed by a valve which
prevent venting after the removal of the syringe. A special inflator with manometer may also
be useful, since the maximal applicable pressure for these cuffs is limited to 15-20 mmHg.
The cuff both retains trickling of saliva, blood, or gastric content into the lung, and inhibits
insufflated air to escape. The control balloon mirrors the pressure of the cuff, therefore
reflects the inflation of the cuff as well.
9. The success of intubation must be verified.
- Comparison of breathing sounds at both medioaxillar lines. If the end of the tube is above
bifurcation, breathing noises are similar over both sides. In case of tube is advanced over the
bifurcation it goes on into the right main bronchial tube usually, therefore breathing sounds
will be much weaker at the left side. In such situation, tube must be pulled back until the
breathing sounds become similar at the sides.
- The simplest method to check the tracheal position of the tube is to push in the upper part of
the thorax and the airflow from the tube is sensible.
- Inflating via the tube the elevation/depression of the thorax may be observable at the level of
the breast.
- Using capnograph the level of ETCO2 expresses the tracheal positioning: if the tube was the
esophagus, the ETCO2 value would be zero.
The clench of the tube may be prevented by the usage of a bite-protector (Guedel-tube or a
wet bandage. The tube, attached to the bite protector is secured to the patient face with an
approx. 30 cm long adhesive plaster forming an X-shaped bandage.
6.19.4. Tubes in the clinical practice
Endothacheal tubes are approx. 30 cm long. Rubber, plastic or latex tubes are used with or
without metal wiring reinforcement (Woodbridge). An inflatable balloon can be found at
one side and is also supplied with another balloon which serves as a pressure/volume
controlling reservoir. The tubes are produced in different width and the outer diameters is
given in Charriére (1 Ch = 1/3 mm) or in millimeters. The ideal size is 36-39 Ch (12-13
mm) for adult men, and 34-36 Ch (11-12 mm) for adult women. Nowadays the inner
diameters are also indicated and whether it is for “oral” or “nasal” use (see below).
Their forms may be conventional, bended, preformed, with or without cuff. The internal hole
is positioned either at the axis and/or at the side. The cuffs may also be different depending on
their sizes and pressure limits. A scale is showing the distance from the top. The X-ray
reflecting marks provide additional help for the proper positioning.
Microlaryngeal tubes represent a unique entity of tubes with their specially formed
transparent body with thin diameter and low-pressure cuff.
The pediatric tubes are made from plastic or rubber and produced without cuff mainly.
Special short tubes are used for tracheostomy (tracheoflex) with special drives and yellowcolored cuffs for striking in case of incipient tube removal.
For the isolated respiration of the lungs, tubes with double lumen and left or right directed
branches (Carlens-, Ravagan-, Robertshow- White- or Bronchopart tubes) are used.
Tube sizes in internal diameter
- 7.5-9 mm for men
- 7.0-8.0 mm for women
- 3.0 mm for prematures (2.5-5 kg)
- 4.0 mm for 1 year old children
- 4.5 mm for 2-3 years
- 5.0 mm for 4-5 years
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6.19.5. Nasotracheal intubation
First, we have to use a nose route with proper diameter and a nose drop to limit mucosal
swelling. After choosing an appropriate nasotracheal tube, the preparations are the same as the
steps of previous method. The tube is carefully introduced into the oropharynx, and then it is
lead through laryngeal gate with laryngoscopic exploration and eye.
6.19.6. Intubation of the awake patient
This can occur if the anesthesia is hard to implement or if the risk of aspiration is increased, if
acute respiratory insufficiency appears with demanding positive-pressure respiration or if the
patient is over-sensitive to relaxant and anesthetics hence quick intubation is need.
If possible, the nasal method is recommended, because patients are able to breathe
spontaneously. Superficial anesthesia is used during the introduction: first the nose, then the
base of the tongue, oropharynx, fossa pyriformis, vocal cord, and pharynx is anesthetized. In
case of females a nasal tube with 7.0 mm diameter and soft-cuff is recommended, while in
case of man the nasal tube diameter is approx. 8.0 mm.
Blind nasotracheal intubation is considered in case of maxillo-facial injuries, neck edema,
intensive care or extreme obesity patients. Nasal way is contraindicated in case of nose
fracture, nose way obstruction or acute sinusitis.
6.19.7. Suction
Suction of the lower portion of the trachea can be easily performed if the patient is
intubated. Suction catheter of a proper size should be introduced and should be pulled out
under continuous suction. Sterility is particularly important. The suction process should
not be last longer than 10-15 seconds after which the patient should be respirated. Under
hypoxic circumstances, the patient should be respirated with oxygen-rich air.
Prior to extubation the pharynx should be suctioned (the area above the balloon) then the
balloon should be deflated and the tube is removed. During this procedure another (nonsterile) suctioning cannula is inserted into the trachea. This removes the accumulated
mucus above the balloon.
6.19.8. Difficulties and obstacles during intubation
Fibrotic stricture and inflammatory occlusion of the oral cavity, biting abnormalities,
everted or loose teeth, palatal fissure, oral, pharyngeal and tongue tumors, mandibular
deformities, jaw ankylosis, tonsillar abscess, goiter, tracheal stricture, neck spondylosis and
the „short thick neck” are the most frequent difficulties.
Apart from deficiencies and defects of the equipment, the position of the patient could cause
difficulties. When relaxation is impossible, muscle tone creates further technical problems.
Risk of aspiration
Duties: respiration through a mask should be avoided, and the mucus or the regurgitated
gastric content should continuously be suctioned. Compression of the cricoid cartilage with
fingers (Sellick- maneuver) can reduce the risk of gastric regurgitation, because this
cartilage presses the underlying esophagus to the vertebra. This procedure is performed by
an assistant during which we conduct the intubation.
6.19.9. Complications
Injuries can occur to the mouth, teeth, mucosa of pharynx and larynx, the vocal cords,
bleeding in the pharynx. Tubes themselves can cause complications. Too thin tube increases
the airway resistance (particularly in children). The tube can get obstructed when it gets
compressed (bitten) by the patient or by excretion, foreign material, or by an over-inflated
balloon. The end of the tube can get into an improper position into the esophagus, into the
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bronchi or can slip out of the trachea. Respiratory obstacles occur when the patient is
coughing, or in case of airways spasm. Rare severe complications are n. recurrens and vocal
cord lesions, subcutaneous and mediastinal emphysema, fibrotic tracheal stricture or rupture.
The overly inflated balloon can cause partial occlusion of the lumen of the tube or if tube is
introduced deeply, only one side of the lungs is respirated (endobronchial intubation).
6.19.10. Intubation of infants
More difficult than that of the adults. This is resulting from anatomical characteristics:
- the epiglottis is located higher
- the glottis aperture is at the level of the third vertebra,
- the epiglottis is longer and steeper,
- the bifurcation is also located higher,
- the narrowest part of the upper airways is the crycoid cartilage and not the vocal split.
Intubation of the infants is performed with tubes without balloon. (The so-called Cole-tube
can be used if its narrow part fits the vocal split. Its wider part is introduced until reaching the
vocal cords, and the narrow distal part will get into the subglottic part of the trachea. Fixation
of the tube is particularly important, because it does not prevent aspiration if it slips back.
Even though we have a tube supplied with a balloon do not inflate it (because of the high
disposition of edema formation at this age). In cases of intubation difficulties, insufficient
equipment, or lack of experience, conicotomy can be recommended.
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