Respiratory management

1. Step Wise Approach in ICU Management of
a Patient in Respiratory Distress:
An Intensivist’s Assessment
Omer Mirza, MD, Intensivist - Covenant HealthCare

2. A THING TO REMEMBER
 An education isn't how much you have committed to memory, or
even how much you know. It's being able to differentiate between
what you know and what you don't know.
 Anatoly France.

3. INTRODUCTION
 Clinical assessment of the acutely unstable patient.
 Noninvasive ventilation.
 High flow nasal cannula.
 Epoprostenol
 Heliox
 And...if we have time.
 Mechanical ventilation.

4. CLINICAL ASSESSMENT OF THE ACUTELY
UNSTABLE PATIENT
 Why do things go wrong in an acutely unstable patient?
 Evaluation of vital organ functions.
 Avoiding typical pitfalls.

5. WHY DO THINGS GO WRONG IN THE
ACUTELY ILL PATIENT?
 Vital functions have not been evaluated.
 Clinical findings cannot be interpreted.
 Search for diagnosis supersedes the evaluation of vital functions.
 There is a discrepancy between working diagnosis and clinical
status, its evolution goes unnoticed.
 Cookbook medicine obscures the importance of evaluation and
support of vital functions.

6. POINTS TO BE CONSIDERED IN THE
EVALUATION OF A POTENTIALLY UNSTABLE
PATIENT.
 Is there dysfunction of vital organs or a high risk for vital
organ dysfunction?
 Are there immediate therapeutic or supportive interventions
needed?
 What is the likely etiology. Is there a specific treatment
available?
 What is the expected clinical course?
 What is the immediate response to therapeutic interventions?
And what is the need for further treatment?
 Where can the necessary treatment best be commenced in
terms of available resources, logistics, and facilities?

7. EVALUATION OF VITAL ORGAN FUNCTIONS
 First question. Is there a problem?
 Is cardiopulmonary resuscitation needed?
 Evaluation of airway and breathing.
 Evaluation of circulation.
 Evaluation of the central nervous system.
 Dysfunction of other vital organs.
 Septic shock.
 Avoiding typical pitfalls.

8. IS CARDIOPULMONARY RESUSCITATION
NEEDED?
 Unconscious, not breathing, no palpable central arterial
pulse.
 No clear contraindication.
 Known living will.
 Documented prolonged lack of circulation.
 Terminal illness.
 Initiate CPR.
 Simple assessment of level of consciousness (verbal and
physical stimulation) simultaneously observing and checking
respiratory movements and airflow and checking the carotid
pulse.

9. EVALUATION OF AIRWAY AND BREATHING
 Is the airway open, and is the patient breathing?
 Is the patient dyspneic? Also search for objective signs of dyspnea.
 Is the patient tachypneic? (or bradypneic)?
 Are breathing movements normal and well coordinated? Are
paradoxical movements present? Does the patient reach a relaxed
end-expiratory volume?
 Does the pulse oximetry suggest hypoxemia? Are the blood gases
abnormal?
 Are the other vital organ functions stable (especially the
cardiovascular and central nervous systems)?

10. CLINICAL ALARM SIGNS – RESPIRATORY
 Tachypnea and increased inspiratory efforts.
 Paradoxical or uncoordinated thoracoabdominal respiratory
movements.
 Use of auxiliary respiratory muscles.
 Concomitant circulatory instability.
 Decreased level of consciousness (preterminal symptom in
respiratory failure)
 Hypoxemia and hypercapnia.
 Hypoxemia and acidosis.
 Hypoxemia and combined respiratory and metabolic acidosis
(preterminal finding).

11. PROBABLE CLINICAL COURSE FOR
RESPIRATORY DYSFUNCTION
 Expected clinical course relevant for planning treatment strategy.
 Rapid recovery scenarios.
 Intoxications and respiratory depression, after general anaesthesia, acute attack of
asthma, cardiogenic acute pulmonary edema, pulmonary embolism.
 Prolonged recovery scenarios.
 Acute lung injury, ARDS, lung contusion, pneumonia induced respiratory
insufficiency, unstable chest wall.

12. EVALUATION OF CIRCULATION.
 Are central pulses present?
 Is the cardiac output low?
 Is the circulation blood volume low, normal, or high?
 Are there symptoms and signs of insufficient tissue perfusion?

13. SIGNS AND SYMPTOMS OF ACUTE
HYPOVOLEMIA (ORDER OF APPEARANCE)
 Tachycardia
 Reduced capillary perfusion.
 Reduced peripheral skin temperature (often a clearly
detectable border between warm and cold skin).
 Decreased venous filling (first in the periphery and then
centrally).
 Oliguria.
 Hypotension.
 Decreased level of consciousness.

14. CLINICAL ALARM SIGNS -
CARDIOVASCULAR
 Hypotension.
 Large respiratory variations of pulse pressure.
 Hypotension and concomitant decreased level of consciousness.

15. PROBABLE CLINICAL COURSE OF
CIRCULATORY DUSFUNCTION
 Rapid recovery scenarios.
 Circulatory failure due to hypovolemia, underlying cause treated. Myocardial
ischemia if addressed by medicines or intervention. Even if due to pulmonary
embolism if treatment commenced early and patient is responsive. Tension
pneumothorax and pericardial tamponade if reversed quickly.
 Prolonged recovery scenarios.
 Pump failure secondary to prolonged ischemia, basic disease that is not rapidly
reversible (myocarditis, vasculitis, acute or chronic heart failure). Septic shock.

16. EVALUATION OF CENTRAL NERVOUS
SYSTEM
 Assess level of consciousness.
 Does the patient appear alert and are the eyes open?
 How big are the pupils are they symmetric and react to light?
 Verbal and motor response check.
 Is it sufficient to protect the airway?
 Hypoxemia, hypercapnea and hypotension can effect neuro
status. Reevaluation after stabilization of circulation and gas
exchange.
 Check hypoglycemia and pCO2 as potentially quickly
reversible.

17. CLINICAL ALARM SIGNS - NEUROLOGICAL
 Acute reduction of level of consciousness.
 New focal neurological signs.
 Stiff neck.
 Glasgow Coma Scale of less than 9 (usually needs intubation for
airway protection).
 Asymmetric pupils. Concern regarding intracranial pathology like
bleed or large stroke.

18. PROBABLE CLINICAL COURSE OF ACUTE
CENTRAL NERVOUS SYSTEM DYSFUNCTION
 Rapid recovery scenarios.
 Intoxications, hypoglycemia, epilepsy, mild brain injury (concussion), transient
ischemia, promptly treated stroke, less severe subarachnoid hemorrhage.
 Prolonged recovery scenarios.
 Prolonged ischemia, infections, severe injuries, metabolic encephalopathies.

19. SEPSIS AND SEPTIC SHOCK
 Wide array of unspecific symptoms and signs.
 Often misinterpreted and often precede acute instability.
 Septic infection produce systemic inflammatory response syndrome.
Not specific to sepsis.
 Symptoms
 Fever, tachycardia, hypotension, impaired capillary perfusion, progressing to
hypovolemia, mental status changes (confusion and agitation), hyperventilation,
dyspnea with hypocapnea and frequently hypoxemia

20. SEPSIS AND SEPTIC SHOCK - 2
 Lab findings.
 Leukocytosis or leukopenia, thrombocytopenia, increased CRP, lactic acid,
metabolic acidosis. Hypothermic, normothermic or febrile.
 Fundamental clinical feature. Septic patient is disproportionately
sick compared to other diagnosis with similar change in vital signs.
 Suspect sepsis in patient with signs of cardiovascular, respiratory or
mental instability.

21. RAPID ASSESSMENT AT BEDSIDE
 Get overall impression of appearance or behavior.
 Speak to patient. Check airflow, observe breathing movements and breath
sounds, check pulses,
 Check control of eye opening, pupil size and reaction, and level of
consciousness.
 Move to patients side and check breathing movements by palpation. Get
an impression of the thorax and abdomen. Evaluate peripheral venous
filling in upper extremities.
 Move to patient legs. Check pulses in femorals, check peripheral venous
filling in feet, edema,
 Can be quickly completed in 30 -60 seconds.

22. NONINVASIVE VENTILATION
 Allows mechanical ventilation without an ET tube.
 Main benefits are decreases in intubation rates, mortality rate, and a
number of infectious complications, particularly pneumonia.
 Well established in COPD exacerbations, improvement in blood
gases and lung mechanics, decrease in rates of intubation,
pneumonia and length of ICU and hospital stay.
 Also established for pulmonary edema. Controversy if better to use
CPAP or PS with PEEP.
 Under study for hypoxemic respiratory failure, immunosuppressed
hypoxemic patients, hasten vent weaning, and to avoid reintubation
after unsuccessful extubation.

23. NIV FOR ACUTE HYPERCAPNIC
RESPIRATORY FAILURE – MECHANISM
 Respiratory failure occurs after a period of rapid shallow
breathing, increasing dead space-to-tidal volume ratio
with subsequent hypoventilation and respiratory acidosis.
 High respiratory centre stimulation together with large
intrathoracic pressure swings generated by respiratory
muscles are insufficient to generate adequate tidal
volumes.
 Rapid shallow breathing facilitate an increase in
pulmonary hyperinflation. This worsens muscle-length
tension.
 All of the above contributes to increasing pCO2 and

24. NIV IN HYPERCAPNIC RESPIRATORY
FAILURE
 Increase in respiratory effort leads to respiratory pump failure
and then eventually respiratory arrest.
 Mechanical ventilation allows rest. Pressure support allows
increased tidal volume with same effort, PEEP (counters auto-
PEEP) reduces patients effort to breathe and markedly
modifies the breathing pattern.
 Increase in tidal volume and decrease in rate improves alveolar
ventilation. Helps decrease the pCO2.
 The pH improvement in the first hours on BiPAP is a success
predictor.

25. NIV IN CARDIOGENIC RESPIRATORY
FAILURE.
 CPAP in cardiogenic respiratory failure improves
oxygenation as it increases functional residual capacity.
 Favorable CPAP hemodynamic effects are decrease in RV
preload, which may increase RV afterload, decreases in LV
preload, decrease in LV transmural pressure, and decrease
in LV afterload.
 With CPAP, improvement in lung compliance, significant
decreases in elastic and resistive components of the work
of breathing, significant reductions in the work of
breathing.

26. INDICATIONS FOR BIPAP
 COPD exacerbation
 Acute pulmonary edema.
 Selected populations of acute respiratory failure
 Other indications
 Facilitation of weaning
 Post operative respiratory failure.
 DNR patients.
 Community acquired pneumonia.
 OSA and OHS patients.

27. CONTRAINDICATIONS FOR NIV
 Non-respiratory organ failure:
 Encephalopathy
 Severe GI bleeding
 Hemodynamic instability with or without cardiac ischemia.
 Facial trauma or surgery.
 Inability to protect airway, risk of aspiration.
 Patient intolerance or uncooperative patient.
 Claustrophobia.

28. TECHNIQUES, EQUIPMENT AND
VENTILATOR MODES
 Full face masks and nasal plugs cause a greater decrease in pCO2
than nasal.
 Nasal masks have greater acceptance.
 Usually pressure support with PEEP.
 May use ICU ventilator.
 Allows patient high control of respiratory rate and timing, inspiratory flow, and tidal
volume.

29. HIGH FLOW NASAL CANNULA
 O2 is typically delivered via low flow systems (nasal cannula or
masks) or high flow systems (venturi masks or non-rebreathers).
 Do not deliver a reliable fraction of inspired O2.
 Poorly tolerated for prolonged periods due to inadequate warming
and humidification.
 Newer systems reliably deliver warmed and humidified O2 at high
flows through nasal cannulae.

30. HIGH FLOW O2 NASAL CANNULA
 Small pliable prongs. Improved comfort.
 Warming and humidification of secretions. Facilitates secretion
removal, prevent desiccation and epithelial injury.
 Washout of nasopharyngeal dead space. Improved washout allows a
higher fraction of minute ventilation to participate in alveolar gas
exchange.
 Continuous positive airway pressure. Buildup of pressure, peak at
end expiration. PEEP effect. Every 10L/min yields 0.7 or 0.35 cm H20
airway pressure.
 High flow rates. Minimal entrainment of room air, more accurate O2
delivery.

31. HIGH FLOW NASAL CANNULA
 Parameters needing to be set.
 FiO2 and Flow rate.
 Indications.
 Not absolute. Tried in various settings. Observational studies. No definite benefit.
 Still used in place of other high flow O2 systems, better tolerated.
 In place of NIV, but unlikely to provide sufficient PEEP in moderate to severe ARDS or
adequate ventilation in patients with hypoventilation. May reduce work of breathing less
than NIV.

32. HIGH FLOW NASAL CANNULA
 Medical patients with severe hypoxemic respiratory failure.
 Improved oxygenation, lower respiratory rate. Decreased MV and comfort.
 Tidal volume unchanged. End-expiratory lung volume and dynamic lung compliance
increased.
 No consistent or convincing benefit in outcomes.
 Post extubation support.
 Post operative respiratory failure.
 Intubation support.

33. HIGH FLOW NASAL CANNULA -
CONTRAINDICATIONS
 Abnormalities or surgery of the face, nose, or airway that preclude
an appropriate-fitting nasal cannula.
 Venous thrombosis. Theoretical. Related to high pressure.
 Abdominal distension, aspiration, barotrauma (rare, pneumothorax).
 Recognition of ARDS may be impacted due to improved p/f ratio.
 Delay in intubation.

34. PULMONARY HYPERTENSION AND POOR
OXYGENATION.
 Epoprostenol. (Flolan, Veletri).
 Strong vasodilator of all vascular beds.
 Potent endogenous inhibitor of platelet aggregation. The
reduction in platelet aggregation results from
epoprostenol's activation of intracellular adenylate cyclase
and the resultant increase in cyclic adenosine
monophosphate concentrations within the platelets.
Additionally, it is capable of decreasing thrombogenesis
and platelet clumping in the lungs by inhibiting platelet
aggregation.

35. VASCULAR ENDOTHELIUM DILATATION
 Hypoxia secondary to ARDS (off-label use):
 Inhalation (off-label): Initial: 0.01 to 0.05 mcg/kg/minute; increase dose in stepwise
fashion based on efficacy and tolerability. Wean by reducing dose by 0.01
mcg/kg/minute every 1 to 2 hours as tolerated.
 Also used in pulmonary hypertension.
 No dosage adjustment for renal or liver abnorm.

36. HELIOX
 Inert, non-toxic gas. Lighter than nitrogen and oxygen.
 Does not enable laminar airflow, it can reduce the airflow
resistance of turbulent flow, as resistance is proportional
to the density of the mixture.
 Potential use in a variety of disease processes
characterized by airflow limitation.
 Optimal helium-oxygen ratio is not known. 80:20/70:30
 Mechanical ventilators have to be recalibrated.

37. Questions?

38. Next Section.
Do we really want to?

39. MODES OF MECHANICAL VENTILATION
 Pressure versus volume ventilation.
 Volume targeting.
 Specific tidal volume is set, flow waveform, and peak flow.
 Focus is on ensuring MV is maintained at target level.
 Pressure targeting.
 Targeted peak airway (= peak alveolar pressure) is set and sometimes inspiratory time.
Tidal volume and gas flow are allowed to vary breath to breath.
 Focus on ensuring targeted alveolar pressure is met but never exceeded.

40. RANGE OF VENTILATOR MODES
 Classic modes
 Assist/control, assist(pressure support) and synchronized intermittent mandatory
ventilation.
 Available for more than 20 yrs.
 New modes
 Designed to improve patient-ventilator synchrony
 Most based on pressure ventilation format.
 Most can be classified as modes that adjust gas delivery within a given breath.
 Computerized control of gas delivery.

41. CONTROL MODE
 Original mode
 Controls all aspect of gas delivery.
 Assumes a passive recipient of mechanical ventilation.
 Nowadays achieved by sedation to apnea in OR by anaesthesia.
 Controlled ventilation is available in both pressure and ventilation
formats.

42. ASSIST / CONTROL MODE
 Essentially control mode with sensitivity set to allow easy patient
triggering of a breath.
 Patient determines respiratory rate.
 Back up to ensure minimum level of ventilation.
 Most commonly used mode.
 Set parameters
 FiO2, back up rate, sensitivity and PEEP .
 Pressure ventilation. Target airway pressure, insp time.
 Volume ventilation. Tidal volume, flow waveform, peak flow and inspiratory time.

43. PRESSURE SUPPORT
 Allows patient greater control over the process.
 Patient triggers a breath and ending is also based on patient
demand.
 Only gas delivery set is pressure level and sensitivity.
 Back up rate is available.

44. SYNCHRONIZED INTERMITTENT
MANDATORY VENTILATION
 Advocates commend benefits of spontaneous breathing between
breaths.
 However, work of breathing can be excessive.
 Respiratory centre has difficulty rapidly changing outputs based on
ventilatory mode.
 May increase patient-ventilator synchrony.

45. PRESSURE-REGULATED VOLUME CONTROL
 Targets both a maximum airway pressure and tidal volume.
 Variation of pressure assist / control.
 Deliver a test breath at low pressure. Measures volume.
 Calculated pressure to deliver targeted tidal volume.
 On every subsequent breath, tidal volume delivered is reassessed.
Pressure is adjusted 0 – 1 cmH2O.
 Concern.
 In patients with a strong drive, and added stimulus of
hypoxemia, fevers, sepsis, etc, patient may get little to
no support inappropriately.

46. VOLUME SUPPORT
 Operates essentially same as PRVC.
 Based on pressure support not pressure assist / control .
 Same assessment breath to breath to assess pressure needed to
deliver targeted tidal volume.
 Same concern regarding too strong a drive.
 Exactly same as setting up pressure support ventilation with
addition of a volume target and maximum pressure.

47. ADAPTIVE SUPPORT VENTILATION
 Very unique mode. Operates on pressure ventilation
format.
 Adjusts ventilator setting for an 'ideal' ventilatory pattern.
 Requiring least amount of patient and ventilator work.
 Goal is to provide preset level of minute ventilation while
minimizing the total work of breathing.
 Provide patients IBW. And % of minimal MV to be
delivered, between 25% to 350%.

48. AUTOMATIC TUBE COMPENSATION
 Sometimes called electronic extubation.
 Resistance properties of all sizes of ET and trach in memory and
continually measuring gas flow.
 Goal is to provide sufficient support during inspiration and
decompression during exhalation to maintain tracheal pressure
equal to baseline.
 Designed only to offload flow resistive properties of the artificial
airway.

49. PROPORTIONAL ASSIST VENTILATION
 Similar to ATC.
 Mechanics of total respiratory system.
 Pressure assist in proportion to patient desired tidal volume and
instantaneous inspired flow.
 Automatically adjusted to meet patient demand.
 Only useful in patients with stable respiratory drives. And an
acceptable respiratory pattern.

50. VOLUME ASSURED PRESSURE SUPPORT
 Also referred to as pressure augmentation.
 Combine initial high flow of a pressure limited breath with constant
volume delivery of a volume targeted breath.
 Differs from PRVC and volume support as it maintains ventilatory
support independent of patient demand.

51. IN CONCLUSION
 How to assess an unstable patient.
 Non-invasive ventilation.
 Modes of ventilation.

52. QUESTIONS?