This document discusses monitoring during mechanical ventilation. There are four key reasons for monitoring: to establish treatment plans, establish trends over time, adjust treatment based on measurements, and set alarms. Various parameters are monitored including vital signs, chest inspection, fluid balance, blood gases, oxygen saturation, end-tidal carbon dioxide, transcutaneous blood gases, and cerebral perfusion pressure. Monitoring provides critical information about a patient's condition and ventilator status to guide care and detect any changes or complications.

1. Monitoring in Mechanical Ventilation
Kamal raj kumar pg- 2

2. Introduction:
Monitoring during mechanical ventilation is vital because clinical status
often changes rapidly and unpredictably.
clinical status may be affected by the underlying illness, medications, organ
failure, and even the settings on the ventilator.
There are four reasons for monitoring a patient
• baseline measurements can be used to establish the initial treatment plan
and serve as a reference point for future measurements;
• a trend can be established to document the progress or regression of a
patient’s condition;
• treatment plans can be added, altered, or discontinued according to the
measurements obtained; and
• high-limit and low-limit alarms can be set on most monitors to safeguard a
patient’s safety.

3. • Vital Signs – HR, BP, RR, TEMP
• Chest Inspection- movement , auscultaion, imaging
• Fluid Balance and Anion Gap
• Arterial Blood Gases- assessment of ventilator status,
oxygenation status, limitation of blood gases
• Oxygen Saturation Monitoring – pulse oximetry accuracy,
clinical use and limitation
• End-Tidal Carbon Dioxide Monitoring – capnography
waveforms, clinical applications , p(a- et )co2 gradient, limitations
and monitoring of capnography
• Transcutaneous Blood Gas Monitoring- transcutaneous po2
and pco2
• Cerebral Perfusion Pressure

4. Vital Signs:
A) Heart Rate: normal 60 – 100 / min
Bradycardia < 60/min Tachycardia > 100/ min
 if appears along with low cardiac Alert clinician to blood volume
output suggest decrease in coronary or cardiac output deficit
blood flow
Often occur with vagal stimulation
during endotracheal suctioning
During suctioning arterial desaturation
& arrhythmias can occur- prevented
by preoxygenation

6. Blood pressure:
• Continuous blood pressure monitoring usually done via
an indwelling arterial catheter interfaced with a pressure monitor.
• The most common insertion site for the catheter is the radial artery.
hypotension
• It is one of the complication of positive pressure ventilation or
peep
• If occurs during mec. Ventn it is ass with excessive intra thoracic
pressure, peak inspiratory pressure and lung volume

8. Respiratory frequency
• Normal – 10-16 breaths / min
• Tachypnea ( > 20 / min ) early warning sign of hypoventilation or
hypoxia
Max. response to hypoxia occurs below a pao2 of 50 mm of hg
• Tachypnea may precede the development of respiratory failure and use of
mechanical ventilation
• During mechanical ventilation, tachypnea is indicative of respiratory
dysfunction
• When tachypnea and low tidal volume are observed in a patient,
successful weaning from mechanical ventilation is not likely
• Rapid, shallow breathing is a reliable sign of ventilatory insufficiency

9. MASIMO RAINBOW ACOUSTIC
MONITORING
Continuous non invasive monitoring
system of respiratory rate

10. Temperature
• Measured @ regular interval or continuously via rectal , esophageal or
pulmonary artery catheter probe
Hyperthermia:
• shifts the oxyhemoglobin
dissociation curve to the
right, causes lower o2
saturation at any pao2 – coz
increased temp promotes
unloading of o2 from hb to
tissue
Hypotheria :
• Seen less common , Lowers persons basal metabolic
rate
• extreme low temperature, hypothermic condition
accounts during management of the ventilator and
patient.
• Eg: the measured PaO2 and PaCO2 values are higher
than the actual values when the sample is collected
under hypothermic conditions, but is analyzed at
body temperature.
• For accurate blood gas values that reflect a patient’s
true ventilatory and oxygenation status, corrections
to the patient’s core temp should be done for blood
gas analysis

11. Hyperthermia Hypothermia
Excessive cooling of phrenic nerve during cab surgery cause
paralysis of hemidiaphragm – temporary cond

12. Chest inspection: • Chest inspection uses indirect methods to assess and
evaluate
the lungs and related structures.
A) Chest Movement : symmetry of each
inspiration depth & rhythm of each tidalvolume cycle
• Symmetry- Chest expansion is symmetrical when the
patient takes in a deep breath and the hands of the
examiner moveapart in equal distance from midline.
• Asymmetrical movement :
bronchial intubation
atelectasis
tension pneumothorax
 if dyssynchronous motion of chest and abdomen
diaphragmatic fatigue / pathology
 affected side – less air movement – consolidation
atelectasis, pleural effusion, pneumothorax

13. Chest inspection:
• B) AUSCULTATION :
Diminished or absent breath sounds
wheezes signs of ventilatory problems
crackles
should be recognized as causes of respiratory distress
A side-to-side technique
of chest auscultation allows
comparison of the quantity of
breath sounds between the
left and right lungs
A cuff leak may be present if
distinct air movement
can be heard toward the end
of a mechanical breath.

15. Auscultation point and there corresponding segments of lung
rt lung
anterior posterior
upper: apical posterior
anterior
Middle: medial
lateral
Lower: anterior superior
posterior
lateral
lt lung
anterior posterior
upper: apical posterior
anterior
lingula –sup
inf
Lower: anterior superior
posterior
lateral
2 10
4
6
8
12
14
16
1
3
5
15
11
13
9
7

16. • Anterior surface Posterior surface Lateral surface

17. Imaging:
A lateral chest radiograph is used in conjunction with the PA radiograph to
verify the location of any abnormal findings
normal
Trachea & mediastinum – midline
Parenchyma – dark & mild
scattered white shadow
Costo phrenic angle – sharp
Abnormal – probable cause
affected side - atelectasis,
Shift pul. Fibrosis
opposite side – tension
pneumothorax
Infiltrates (large white shadow)
suggest secretions, atelectasis
Blunted – accumulation of fluid in
pleural space ( pleural effusion ,
hemothorax, empyema)

18. Bony structure – smooth &cont.
Cardiac shadow
< 50 %
b/w rt & lt cp angle
 jagged appearance - # bones
 cardiac shadow > 50 % - congestive
heart

19. Fluid balance :
• positive pressure vent. Cardiac out put
hence renal perfusion
• Mechanical vent. ADH
ANF
• Normal urine output is 50 to 60 mL/hour
• Urine output of below 20 mL/hour (or 400 mL in a 24-hour period or 160
mL in 8 hours) is indicative of fluid deficiency ( oliguria )
• Oliguria may be seen after bleeding, diarrhea, renal failure, shock, drug
poisoning, deep coma, or hypertrophy of the prostate.
decreased
fluid output &
fluid retention

20. Anion gap : cations (Na , K ) - anions ( Cl, HCO3 ) in the plasma.
normal range is 15 to 20 ( K+ included), 10 to 14 mEq/L (K+ excluded).
NAGMA
• Caused by a loss of base
• hyperchloremic metabolic
acidosis
HAGMA
• Due to increased fixed acids
• Acids may be produced biologically
(lactic acidosis, renal failure , DKA)
• From external source (salicylate &
alcohol poisoning)
Respiratory Compensation for Metabolic Acidosis.
• Hyperventilation ( PaCO2) may occur as a compensatory mechanism for met.
acidosis
• This should not be assumed as respiratory insufficiancy( primary alveolar
hyperventilation)
• the ventilator frequency must not be reduced due to an abnormally low PaCO2.
Otherwise, persistent hyperventilation and worsening of the work of breathing will
continue due to a sudden decrease of ventilator frequency

21. • In case of ,
Severe K+ depletion can lead to metabolic alkalosis
and compensatory hypoventilation
This may prolong the weaning process when mechanical
ventilation is needed to supplement the decreasing
spontaneous ventilation.

22. ARTERIAL BLOOD GASES
A) Assessment of Ventilatory Status :
frequency or tidal volume
Hypoventilation & respiratory acidosis - increase
Hyperventilation &respiratory alkalosis - decreased
Metabolic disturbances - no changes
Aprolongedincreaseintheworkofbreathingmayleadtorespiratorymusclefatigueand
ventilatoryfailure ( > 10 lts/min of min ventilation ass. with poor prognosis)

23. B) Assessment of Oxygenation Status:
(1) arterial oxygen tension (PaO2),
(2) alveolar-arterial oxygen tension gradient [P(A-a)O2],
(3) arterial to alveolar oxygen tension ratio (PaO2/PAO2),
(4) PaO2 to FIO2 ratio
• PaO2 is obtained from arterial blood gas analysis
• PAO2 can be calculated by
• R is respiratory quotient (estimated to be 0.8 and it may be
deleted from equation when the FIO2 is greater than 60%).
• A decrease in PaO2 with little or no increase in P(A-a)O2 is
probably due to hypoventilation- confirmed by an elevated PaCO2
• acute hypoventilation respiratory acidosis
Tissue hypoxia

25.  a decrease in PaO2 with concurrent increase in P(A-a)O2 is indicative of
hypoxemia due to diffusion defect, V/Q mismatch, or shunt
Diffusion defect: impaired gas exchange through alv-capillary memb.
(1) low oxygen pressure gradient,
(2) increased alveolar-capillary thicknessor diffusion gradient,
(3) decreased alveolar surface area
When the PaO2 is decreased with little or no change in PaCO2,
V/Qmismatch or intrapulmonaryshunt should be suspected.
V/Q mismatch: responds moderately to
High V/Q is related to deadspace ventilation,
low V/Q is associated with intrapulmonary shunting.
Intrapulmonary shunt: will not respond to supplement oxygen,
peep and oxygen are required to correct hypoxemia

26. Limitations of Blood Gases
• Skillfull work of arterial puncturing & catheter placement
• introduction of air bubbles while talking sample
• Exessive dilution with heparin – inaccurate results
• Gives isolated measurement in time rather than trend – hence should
be used along with non invasive monitoring device like puse oximetry
• Abg is late indicator of respiratory failure and has limited use in early
warning signs

27. OXYGEN SATURATION MONITORING
The arterial oxygen saturation (SaO2) is best but not readily available.
• A simple and noninvasive method to monitor the oxygen saturation is by using a
pulse oximeter. The pulse oximetry measures oxyhemoglobin saturation (SpO2) is
less accurate than SaO2
Pulse Oximetry :works by emitting dual wavelengths of light through a pulsating
vascular field.
Note: The SpO2 reading should not be used and reported if a concurrent low
perfusionalarm is present
Accuracy :Oxygenation of ventilator-dependent patient- assured when the SpO2 is
kept > 92% as this level correlates with a PaO2 > 60 mm Hg
Limitation: SpO2 becomes less accurate as SaO2 decreases & over estimation of
a patient’s oxygenation status may result
• low perfusion states and presence of dyshemoglobins maylead to SpO2
measurements that are higher than the actual SaO2

29. END-TIDAL CARBON DIOXIDE MONITORING
• Capnography : measurement of the
partial pressure of carbon dioxide in a
gas sample , collected at the end of
expiration, it is called
end-tidal partial pressure of carbon
dioxide (PetCO2)
• techn : infrared absorption by main
stream or side stream sensor

30. Capnography wave forms & clinical app
normal :

31. Abnormal wave forms:

32. P(a-et)CO2 Gradient:
• Normal value – 2 mm of hg , critically ill – 5 mm of hg acceptable
• primarily affected by alveolar deadspace ventilation, old age, presence of
pulmonary disease, and changes in mechanical volume and modality

33. Limitation of capnography:
• Capnography readings reflect only the changes in a patient’s ventilatory
status, rather than the improvement or deterioration of the patient
• Eg: pulmonary embolism - in decrease in PetCO2 due to physiologic
deadspace ventilation so don’t ventilator frequency
• Other conditions which physiological dead space are
- hypotension
- high intra thoracic pressure secondary to mv

34. Transcutaneous blood gas monitoring: in infants
Transcutaneous PO2 (PtcO2)
• miniature Clark (PO2) electrode on
the skin via a double-sided adhesive
• Combined platinum & silver electrode
• used as an indicator of hypoxemia
• The clinical optimal range of PtcO2 for
most infants is 50 mm Hg to 70 mm Hg
• Limitation: Accuracy of the PtcO2
electrode is affected by skin edema,
hypothermia,and capillary perfusion
status
• Need to change frequently (4 hours) to
avoid erythemia and burns
Transcutaneous PCO2 (PtcCO2)
• Severinghaus (PCO2) electrode on
the skin via a double-sided adhesive
• Limitations : PtcCO2 values are
usually higher than PaCO2 values
• due to increased CO2 production as
underlying tissues are heated
• during shock or low perfusion states,
the PtcCO2 measures higher than
the actual PaCO2 due to increased
accumulation of tissue CO2

35. CEREBRAL PERFUSION PRESSURE
• pressure required to provide blood flow, oxygen, and metabolites to the brain ,
normally auto-regulated
• CPP = MAP(70 – 100) - ICP (8 – 10); normal range – 70 to 80 mm of hg
• Auto regulation lost - head injury , where cerebral vascular resistance
Brain – becomes vulnerable to chnaging bp
• on degre of decrease in cerebral perfusion – ischemia / brain death
• critical threshold is believed to be from 70 to 80 mm Hg.
• Mortality increases about 20% for each 10 mm Hg drop in CPP
• 35% reduction in mortality was achieved when the CPP was maintained above
70 mm Hg

36. Relationship of map and icp with cpp:
• High cpp can be maintained by map or by icp
• Usually icp is controlled i.e < 20 mm of hg, so main stay of
managing is by raising map
• Map is managed,
initially – adequate fluid balance
then if needed – vaso pressors ( nor epinephrine or dopamine)
patients with severe brain injury, systemic hypotension
contributes to an increased morbidity and mortality