Hypoxemic PaO2 < 60 mmHg Hypercapnic PaCO2 > 45 mmHg
Hypercapnic respiratory failure
Decreased minute ventilation
Stroke, brain tumor, spinal cord lesions, drug overdose
Peripheral nerve disease
Muscular dystrophy, respiratory muscles fatigue
Chest wall abnormalities
Scoliosis, kyphosis, obesity
Airway obstruction Upper airway obstruction, Asthma, COPD
Ventilatory demand depends on
dead space and minute ventilation
Ventilatory supply depends on
Muscle /neuron function
Indication/contraindication of OLV
Physiology changes of OLV
Selection of the methods for OLV
Management of common problems associated with OLV, especially hypoxemia
One-lung ventilation, OLV, means separation of the two lungs and each lung functioning independently by preparation of the airway
Protection of healthy lung from infected/bleeding one
Diversion of ventilation from damaged airway or lung
Improved exposure of surgical field
More manipulation of airway, more damage
Significant physiologic change and easily development of hypoxemia
Isolation of one lung from the other to avoid spillage or contamination
Control of the distribution of ventilation
Bronchopleural cutaneous fistula
Surgical opening of a major conducting airway
giant unilateral lung cyst or bulla
Tracheobronchial tree disruption
Life-threatening hypoxemia due to unilateral lung disease
Unilateral bronchopulmonary lavage...
Variations of pao2 <3-4 mm hg and even less for paco2
To expend minimal energy in the work of breathing
chest wall and muscle receptors
aortic bodies (significance ?)
bifurcation of common carotid
blood supply-external carotid
venous drain-int jugular
nerve supply- ix nerve
rich blood supply(2l/100g/min)
utilizes dissolved o2 from blood unlike other tissues
senses changes in pa o2
hence not affected by conditions in which pao2 (n)
•Spatial & anatomical variation
•Rate of alveolar filling
•Rate of alveolar emptying
Clinical relevance Clinical relevance
Perfusion is poor & pulsatile at apex
Pa& Pv proportionately increases from top to bottom
PA changes minimally with gravity
Pressures are max at bottom
Pulmonary edema starts at bottom
Redistribution of blood flow to apex –antler’s horn
Understanding V/Q relationships Understanding V/Q relationships
Consider lung as single unit
– Relationships between PAO2, PACO2, alveolar ventilation & pulmonary blood flow
–Alveolar gas equation
Consider lung as multiple units of varying V/Q
–Clinical consequences in health & disease
Alveolar PO and PCO Alveolar PO2 and PCO2
Determined by the ratio between ventilation and blood flow: V/Q
PO2and PCO2 are inversely related through alveolar ventilation
Increasing V/Q produces higher PAO2and lower PACO2
Decreasing V/Q produces lower PAO2and higher PACO2
Lung -First barrier between the body and its surrounding atmosphere.
Variousactivitiesexposehumanstodifferentenvironmentsinwhich Various activities expose humans to different environments in which the stresses are beyond our physiologic capabilities.
Extreme environments & the lung
Lung physiology in diving
Diving -Exposure to higher than normal ambient pressure.
Compression, isobaric, and decompression phases.
One atmosphere -760 mm Hg or 101.3 kPa.
One bar corresponds to a pressure of 750 mm Hg, 100 kPa, or 10 msw(Metres of sea water).
Depth of 30 msw-pressure of 4 bars
100 mswpressure equivalent of 11 bars.
4 bars / 30 msw, the fractional concentration of oxygen is still 0.21 but the partial pressure is 84 kPa
Pulmonary baro trauma(PBT)
Exposure to abrupt pressure changes. posuetoabuptpessuecages
IndividualsatriskofPBT-Astronauts,aviators, Individuals at risk of PBT Astronauts, aviators, compressed air workers, and divers.
Diving related PBT –Second among all causes of SCUBA diving fatalities.
PBT during descent of apnoeadive -Lung gg squeeze
PBT during ascent
lung volumes measured by spirometry are useful for detecting, characterising & quantifying the severity of lung disease
Measurements of absolute lung volumes, RV, FRC g,, & TLC are technically more challenging --->limiting use in clinical practice
Precise role of lung volume measurements in the assessment of disease severity, functional assessment of disease severity, functional disability, course of disease and response to treatment remains to be determined
Lung volume are necessary for a correct physiological diagnosis in certain clinical conditions
Contrast to the relative simplicity of spirometric volumes variety of disparate techniques have volumes variety of disparate techniques have been developed for the measurement of absolute lung volumes
Various methodologies of body plethysmography, nitrogen washout, gas dilution, and radiographic imaging methods
Basic Lung Volumes
The amount of gas inspired or expired with each breath
Inspiratory Reserve Volume
Maximum amount of additional air that can be inspired from the end of a normal inspiration
Expiratory Reserve Volume
The maximum volume of additional air that can be expired from the end of a normal expiration
The volume of air remaining in the lung after a maximal expiration
This is the only lung volume which cannotbe measred ith a spirometer
2.Diffusion of O2& CO2
3.Transport of O2& CO2
4.Regulation of respiration
Movement of air in & out of lungs the
dead space ventilation
Measurement of ventilation
The work of breathing
Importance in the ICU
Importance in the ICU
Measurement of WOB in ICU not routine
Until recently performed by physiologists>clinicians
Most ICU pts. are extubated < 96 hrs using standard weaning criteria
“advantages” of measuring WOB
ensure pt.-vent synchrony
aid to weaning
comparison of diff. modes of MV
Unwarranted thrombolytic therapy
Unnecessary emergency angiography
Unnecessary anxiety (for intern)
Normal ST elevation
1 - 3mm elevation in one or more precordial leads in relation to the end of the PR segment (male pattern)
ST segment is concave
Most commonly the ST-segment elevation is most marked in V4 with a notch at the J point, and the ST segment is concave
T waves are tall and are not inverted
This normal variant differs from the early-repolarization pattern in that the T waves are inverted and the ST segment tends to be coved
Combination of an early-repolarization pattern and a persistent juvenile T-wave pattern. Often, the findings are so suggestive of acute myocardial infarction that an echocardiogram is necessary to differentiate them, especially if one is not aware of this normal variant. In most cases of this normal variant, the QT interval is short, whereas it is not short in acute infarction or pericarditis.
Deep S wave
QS pattern in leads V1 through V3
Elevated ST segment is concave in a pt with uncomplicated LV hypertrophy as compared with convex in a pt with acute concomitant MI
Left Bundle Branch Block
Making the dx of acute infarction in the presence of LBBB can be problematic, since the ST segment is either elevated or depressed secondarily, simulating or masking an infarction pattern
Sgarbossa’s criteria is controversial and has not been validated
Calculate the anion gap
Calculate the delta gap
Differentials for specific acid-base disorders
Steps for ABG analysis
What is the pH? Acidemia or Alkalemia?
What is the primary disorder present?
Is there appropriate compensation?
Is the compensation acute or chronic?
Is there an anion gap?
If there is a AG check the delta gap?
What is the differential for the clinical processes?
Acute: for every 10 increase in pCO2 -> HCO3 increases by 1 and there is a decrease of 0.08 in pH MEMORIZE
Chronic: for every 10 increase in pCO2 -> HCO3 increases by 4 and there is a decrease of 0.03 in pH
Acute: for every 10 decrease in pCO2 -> HCO3 decreases by 2 and there is a increase of 0.08 in PH MEMORIZE
Chronic: for every 10 decrease in pCO2 -> HCO3 decreases by 5 and there is a increase of 0.03 in PH
Winter’s formula: pCO2 = 1.5[HCO3] + 8 ± 2 MEMORIZE
If serum pCO2 > expected pCO2 -> additional respiratory acidosis
For every 10 increase in HCO3 -> pCO2 increases by 6
Provides extensive gas exchange surface area between air and circulating blood
Moves air to and from exchange surfaces of lungs
Protects respiratory surfaces from outside environment
Participates in olfactory sense
Regulation of breathing
Medullary rhythmicity center
Nerves extend to intercostals and diaphragm
Signals are sent automatically
Expiratory center is activated during forced breathing
Controls degree of lung inflation; inhibits inspiration
Breathing can be controlled voluntarily, up to a point
Too much CO2 and H+ will stimulate inspiratory area, phrenic and intercostal nerves
Central chemoreceptors: medulla oblongata monitors CSF
Aortic bodies (vagus nerve)
Carotid bodies (glossopharyngeal nerve)
Respond to fluctuations in blood O₂, CO2 and H⁺ levels
Pulmonary stretch receptors prevent over inflation of lungs (promote expiration
4 Pulmonary Volumes
Resting tidal volume:
in a normal respiratory cycle
Expiratory reserve volume (ERV):
after a normal exhalation
after maximal exhalation
minimal volume (in a collapsed lung)
Inspiratory reserve volume (IRV):
after a normal inspiration..
Usually preceded by physiological deterioration,
although it can occur suddenly in stable patients
Specific causes of cardiac arrest (all potentially reversible):
tamponade, hypovolemia, myocardial ischaemia, pacing failure,
or tension pneumothorax
Cardiac arrest after cardiac surgery:
If treated promptly survival rate is relatively high.
Rate of survival to hospital discharge is 54% to 79% in adults and 41% in children.
Key to the successful resuscitation of cardiac arrest in these patients is to perform emergency resternotomy early, especially in the context of tamponade or haemorrhage, where external chest compressions may be ineffective.
Cardiac arrest is defined as the absence of any spontaneous circulation:
MAP < 30 mmHg
Near cardiac arrest is defined as:
MAP 30 - 50 mmHg
Most common causes of cardiac arrest after cardiac surgery:
Initial resuscitation algorithm:
Confirm that hypotension or cardiac arrest is real
Ensure airway / ventilate with manual resuscitator
Avoid prolonged attempts at intubation
Exclude tension pneumothorax
Briefly disconnect pacer to R/O VF
Discontinue hypotensive agents and sedatives
Ensure vasoactive drugs are being delivered
Consider early chest reopening in all patients
Autonomic nervous system
Accelerated junctional rhythm
Paroxysmal supraventricular tachycardia
Ectopic atrial tachycardia
Low cardiac output
Treatment directed at the underlying cause
Must be distinguished from other narrow-complex tachycardias
Atrial electrogram (AEG) when diagnosis is uncertain
Connect the left & right arm ECG cables to the atrial pacing wires
Alternatively, connect the V lead to one atrial pacing wire
Atrial Electrogram (AEG):
AEG are useful for differentiating supraventricular arrhythmias.
Atrial fibrillation with RVR > 150 bpm, the rhythm may be misdiagnosed as paroxysmal SVT.
Atrial flutter: atrial activity may not be obvious on the surface ECG.
In patients with preexisting bundle-branch block, the development of a postoperative SVT may be difficult to distinguish from VT.
An accurate diagnosis can be readily made if an atrial electrogram (AEG) is recorded.