Pathophysiology of hypercapnic and hypoxic respiratory failure

Posted by e-Medical PPT Thursday, May 14, 2015 0 comments

Respiratory Failure inadequate blood oxygenation or CO2 removal A syndrome rather than a disease
Hypoxemic PaO2 < 60 mmHg Hypercapnic PaCO2 > 45 mmHg

Hypercapnic respiratory failure
Decreased minute ventilation †
CNS disorders „
Stroke, brain tumor, spinal cord lesions, drug overdose †
Peripheral nerve disease
„ Guillain-Barresyndrome, botulism,
myasthenia gravis †
Muscle disorders
„Muscular dystrophy, respiratory muscles fatigue
Chest wall abnormalities „
Scoliosis, kyphosis, obesity †
Metabolic abnormalities „
Myxedema, hypokalemia †
Airway obstruction „Upper airway obstruction, Asthma, COPD

Ventilatory demand depends on
O2 demand
dead space and minute ventilation

Ventilatory supply depends on
Respiratory drive
Muscle /neuron function
Respiratory mechanics

Use of One-Lung Ventilation for Thoracic Surgery

Posted by e-Medical PPT Tuesday, May 12, 2015 0 comments

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
OLV provides:
Protection of healthy lung from infected/bleeding one
Diversion of ventilation from damaged airway or lung
Improved exposure of surgical field
OLV causes:
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
Massive hemorrhage
Control of the distribution of ventilation
Bronchopleural fistula
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...

Control of Respiration

Posted by e-Medical PPT Saturday, May 9, 2015 0 comments

Ventilation is constantly adjusted to maintain the homeostasis of bld gases and arterial ph
Variations of pao2 <3-4 mm hg and even less for paco2
To expend minimal energy in the work of breathing

peripheral chemoreceptors
central chemoreceptors
pulmonary receptors
chest wall and muscle receptors

Peripheral chemoreceptors
carotid bodies
aortic bodies (significance ?)
bifurcation of common carotid
blood supply-external carotid
venous drain-int jugular
nerve supply- ix  nerve

Carotid body
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)
mild anemia
co poisoning..

Ventilation‐perfusion in health & disease

Posted by e-Medical PPT Thursday, May 7, 2015 0 comments

Distribution of ventilation Distribution of ventilation
•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 in extreme environments

Posted by e-Medical PPT Monday, May 4, 2015 0 comments

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
High altitude

Extreme cold

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

Measurement of Lung Volumes and Airway Resistance

Posted by e-Medical PPT Sunday, May 3, 2015 0 comments

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
Tidal Volume
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
€Residual Volume
The volume of air remaining in the lung after a maximal expiration
ƒThis is the only lung volume which cannotbe measred ith a spirometer

Physiology of ventilation & work of breathing

Posted by e-Medical PPT Saturday, May 2, 2015 0 comments

Goals of respiration
2.Diffusion of O2& CO2
3.Transport of O2& CO2
4.Regulation of respiration

Movement of air in & out of lungs the
    respiratory muscles
    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


Posted by e-Medical PPT Thursday, June 26, 2014 0 comments

Recognize ST segment elevation in conditions other than acute MI

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

Early Repolarization
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

T-wave Inversion
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.

LV Hypertrophy
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

ABG analysis & Acid-Base Disorders

Posted by e-Medical PPT Tuesday, June 24, 2014 0 comments

Discuss simple steps in analyzing ABGs
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?

Respiratory Acidosis
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
Respiratory Alkalosis
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

Metabolic Acidosis
Winter’s formula: pCO2 = 1.5[HCO3] + 8 ± 2 MEMORIZE
If serum pCO2 > expected pCO2 -> additional respiratory acidosis
Metabolic Alkalosis
For every 10 increase in HCO3 -> pCO2 increases by 6

5 Functions of the Respiratory System
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
Produces sounds
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
Pneumotaxic area
  Controls degree of lung inflation; inhibits inspiration
Apneustic area
  Promotes 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

Peripheral chemoreceptors
Aortic bodies (vagus nerve)
Carotid bodies (glossopharyngeal nerve)
Respond to fluctuations in blood O₂, CO2 and H⁺ levels
Rapid respond
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
Residual volume:
 after maximal exhalation
 minimal volume (in a collapsed lung)
Inspiratory reserve volume (IRV):
 after a normal inspiration..


Posted by e-Medical PPT Wednesday, January 8, 2014 0 comments

Cardiac arrest following major cardiac surgery: 0.7-2.9%
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
    non-pulsatile waveform

Near cardiac arrest is defined as:
    MAP 30 - 50 mmHg
    pulsatile waveform

Most common causes of cardiac arrest after cardiac surgery:
Ventricular fibrillation
Cardiac tamponade

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


Posted by e-Medical PPT Wednesday, January 1, 2014 0 comments

Proarrhythmic factors:
Autonomic nervous system
Myocardial ischemia
Myocardial Infarction
Proarrhythmic drugs

Narrow-complex tachycardias:
Sinus tachycardia
Atrial fibrillation
Atrial flutter
Accelerated junctional rhythm
Paroxysmal supraventricular tachycardia
Ectopic atrial tachycardia

Pain, anxiety
Surgical stress
Low cardiac output
Myocardial ischemia
Catecholamine administration

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.

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