PHYSIOT IN ICU Flashcards
- 3 main causes of ICU stress
- psychological torture
- examples of conditions
- pain, lack of sleep & intubation
- sensory & sleep deprivation, psychotropic drugs, prolonged immobility, isolation & reduced communication
- communication difficulty, uncertainty & anxiety, sleep fragmentation, fear, sensory deprivation, sensory overload, disorientation, depersonalization & delirium, sensory monotony & loss of time sense, discomfort, pain, helplessness, dependency & depression, loss of privacy, dignity & identity
Goals of PT in ICU
Early mobilization
Optimize perfusion
Optimize ventilation
EARLY MOB: when? How? Do not forget
WHEN
- Starting right at beginning after admission to ICU (first days) to mobilisation / physical exercise
- Evidence +++
- Feasible & safe even if patient monitored with various devices (mechanical ventilation, sedation, dialyses..)
HOW
- Start as soon as possible (if no red flag)
- Incite to minimal sedation (drug level)
- If sedated : passive mobilisation should be started
- Prescription depending on abilities of each patient : active or passive techniques, in or out of bed
- Specific skills :
‣ Physiotherapists : walking, specific mobilisations, use of motorised machines (cyclo- ergometers, etc.)
‣ All ICU team : patient positioning, transfer out of bed - At least 5/7 days
Top 5 of better things to do
DO NOT FORGET
- Communication : mobilisation sessions organized in agreement with whole ICU team
- Some techniques (verticalization, transfer, walking session..) require several people (at least PT + someone else)
- Adapt required ventilatory parameters during & after mobilisation session
- Machines/devices cleaned after use
Team work to avoid complications
Team work to execute maneuver correctly
VITAL SIGNS: monitoring, conscience level (scale) & delirium
Be careful of every invasive and non-invasive devices before the intervention
• Continuous monitoring of vital signs during the mobilisation • Consider individualised criteria to stop the mobilisation. i.e : • 35>HR>130
• MAP < 65 mmHg
• BF(RR)>35
• SaO2 < 88%
• Pain (VAS) > 5
Glasgow Coma Scale
Picture
MECHANICAL VENTILATION: respi failure I & II, values & 2 ≠ types
- PaO2<60
- Pa CO2>50
- SpO2<88%
- F>30-35 mpm
- PaO2/FIO2 (%)< 150-200
LUNG FAILURE
= white lung (hypoxemia) - Pneumonia
- Pulmonary edema
- ARDS
PUMP FAILURE
= black lung
- COPD
- Asthma
- Neuromuscular disease
MECHANICAL VENTILATION: types
NEGATIVE PRESSURE
- “Iron Lung”
- First used in 1928
- Poliomyelites outbreak (1940- 1950)
Disadvantages
- Patient in a box => no mobilization
POSITIVE PRESSURE
- Invasive or Non Invasive
- Invasive first used in 1955
- Modern standard of Mechanical Ventilation
MECHANICAL VENTILATION: indications
RESPIRATORY FAILURE
- Apnea / Respiratory Arrest
- Inadequate ventilation (acute vs. chronic) - Inadequate oxygenation
- Chronic respiratory insufficiency with FTT - Protect upper airways
CARDIAC INSUFFICIENCY
- Eliminate work of breathing - Reduce oxygen consumption
NEUROLOGIC DYSFUNCTION
- Central hypoventilation/ frequent apnea - Patient comatose, GCS < 8
- Inability to protect airway
- Confort/ Sedation
MECHANICAL VENTILATION: modes
Controlled mode:
- Pressure & volume: every breath fully supported (controlled) by ventilator
- Every breath fully supported by ventilator in pure control modes, patients unable to breathe except at controlled set rate
Assisted-Controlled Ventilation:
- Minimum set rate & all triggered breaths above that rate also fully supported. They can be synchronized to patient or not:
IMV Modes:
- Intermittent mandatory ventilation modes
- Breaths “above” set rate not supported (mode outdated)
SIMV:
- Ventilator synchronizes IMV “breath” with patient’s effort (works better when Ventilator = micro-processed)
- Minimum resp rate is set
Pressure Support:
- Ventilator supplies pressure support but no respiratory rate - Pressure support fixed or variable (volume support, volume assured support..)
IMV & SIMV = assisted mode
It’s not machine which do that BUT machine push patient to do that
MECHANICAL VENTILATION: weaning
Weaning from mechanical ventilation = process of reducing ventilatory support, ultimately resulting in patient breathing spontaneously & being extubated
- Process achieved rapidly in 80% of patients when original cause of respiratory failure improved
- Process standardized
MECHANICAL VENTILATION: complications & respi mecha
- Over distention of alveoli
- Compression of lungs
- Spontaneous breathing vs mechanical ventilation
MECHANICAL VENTILATION: manipulation
- Minute Ventilation (increase respiratory rate, tidal volume)
- Pressure Gradient = A-a equation (increase atmospheric pressure, FiO2, increase ventilation, change RQ RQ = CO2 eliminated / O2 consumed)
- Surface Area = volume of lungs available for ventilation (increase volume by increasing airway pressure.. mean airway pressure)
- Solubility = perflurocarbons
- Ventilators deliver gas to lungs using positive pressure at certain rate (respiratory frequency,volume & pressure)
- Amount of gas delivered limited by time, pressure or volume (respiratory frequency, volume & pressure)
- Duration cycled by time, pressure or flow
If volume is set, pressure varies
If pressure is set, volume varies
=> according to compliance
COMPLIANCE = D Volume / D Pressure
POSITIVE END EXPIRATORY PRESSURE (PEEP): def, adjustments & exceptions
D = positive pressure that remain in airways at end of respiratory cycle (end of exhalation) that is greater than atmospheric pressure in mechanically ventilated patients
A: - Used to help prevent alveolar collapse at end inspiration - Also used to recruit collapsed lung spaces or stent open floppy airways
E: Is it really that simple ?
- Increasing PEEP can increase dead space, decrease cardiac output, increase V/Q mismatch
- This increases RA pressure & decreases venous return, & preload
- Decreases cardiac output: less blood in RV means less blood reaching LV & less blood that can be pumped out
- Decreased preload means that heart works at less efficient point, generating less effective work
- Result = drop in mean arterial pressure (MAP)
NON INVASIVE VENTILATION: definition & goals, indications & types
D: = delivery of mechanical ventilation to lungs using techniques that do not require invasive artificial airway (endotracheal tube, tracheostomy)
Goals:
- Provide time for cause of respiratory failure to resolve & improve gas exchange
- Overcome auto-PEEP
- Unload respiratory muscle
- Decrease dyspnea
- Avoid Endotracheal Intubation
- Avoid complications
To use that device, diaphragm of patient needs to work Wait 20min to 1h to see improvements
I: Strong Evidence (RCTs):
- COPD exacerbations
-Acute Cardiogenic Pulmonary edema - Immunocompromised Patients
Less Strong Evidence (Single controlled trials and Case Series):
- Asthma
- Community acquired pneumonia (COPD)
- Post operative Respiratory Failure
- Facilitation of weaning in COPD patients - Do not intubate patients
Weak Evidence (few case series, case reports): -Cystic Fibrosis
- Community acquired pneumonia (non- COPD) - Upper Airways obstruction
T: Negative Pressure NIV
- Main means of NIV during early 1900’s
- Extensively used during polio epidemics
- Tank ventilator “iron lung”
- Cuirass, Jacket ventilator, Hayek oscillator
Positive Pressure NIV
- Positive pressure delivered through mask - CPAP
- BIPAP
- AVAPS
- ASV
NON INVASIVE VENTILATION: advantages, disadvantages & contraindications
A: - Noninvasive
- Correction of gas exchange
- Improve lung mechanics
- Reduce resistive work imposed by invasive ventilation
- Ventilates effectively with lower pressures
- Flexibility in initiation/termination
- Intermittent application
- Patient comfort
- Correct mental status speech/swallowing expectoration
- Reduces need for nasogastric tubes - Reduce need for sedation
‣ Avoids complications of ETT
‣ Trauma/injury, aspiration
- Avoids complications of invasive ventilation ‣ Infection-pneumonia, sepsis, sinusitis
‣ GI bleed
‣ DVT - Less cost
- Decrease mortality associated with respiratory failure
HOW DOES IT WORK?
- Reduction in inspiratory muscle work & avoidance of respiratory muscle fatigue
- Augments tidal volume
- Improves compliance by reversing
microatelectasis
- Overcome intrinsic PEEP
- Enhanced cardiovascular function (afterload reduction) - Stent airway
- Reduce CO2 production
FOR HYPOXEMIC RESPIRATORY FAILURE
- Increased FIO2
- PEEP effect
• Alveolar recruitment
• Increased V/Q
• Decreased Shunt
• Increased FRC
• Decreased RR and WOB
• Offsets auto-PEEP
• Reduce airway resistance • Improve VT, VE, PaCO2
TYPES
Negative Pressure NIV
- Main means of NIV during early 1900’s
- Extensively used during polio epidemics
- Tank ventilator “iron lung”
- Cuirass, Jacket ventilator, Hayek oscillator
Positive Pressure NIV
- Positive pressure delivered through mask - CPAP
- BIPAP
- AVAPS
- ASV
OBSTRUCTIVE SLEEP APNEA
Use for patient with obstructive sleep apnea
‣
Assist in end of life care
D: System
- Slower correction of gas exchange abnormalities
- Time commitment/attention
- Gastric distention
Interface
- Leaks
- Skin necrosis/rash - Eye/ear irritation - Sinus pressure
Airway
- Aspiration
- Limited secretion clearance
C: Cardiopulmonary arrest
- Hemodynamic instability
- Nonrespiratory multiorgan failure - Mental status change
‣ Uncooperative
‣ Encephalopathy (GCS <10) ‣ Seizure
- Inability to protect airway ‣ Secretions
- Recent Trauma
‣ Facial/angioedema
‣ Upper airway surgery
- Facial deformities - +/-edentulous
- GI Bleed/surgery
- Intractable emesis - Tumors:
‣ Head/neck
‣ Extrinsic compression of airway - Airway obstruction
- Recent neurosurgery
- Burns
- Untreated pneumothorax
NON INVASIVE VENTILATION: how work? For hypoxemic respi failure, for which other disease
How work? - Reduction in inspiratory muscle work & avoidance of respiratory muscle fatigue
- Augments tidal volume
- Improves compliance by reversing
microatelectasis
- Overcome intrinsic PEEP
- Enhanced cardiovascular function (afterload reduction) - Stent airway
- Reduce CO2 production
Hypoxemic: - Increased FIO2
- PEEP effect
• Alveolar recruitment
• Increased V/Q
• Decreased Shunt
• Increased FRC
• Decreased RR and WOB
• Offsets auto-PEEP
• Reduce airway resistance • Improve VT, VE, PaCO2
Obstructive sleep apnea
AIRWAY CLEARANCE: when? How? Do not forget? Monitoring
W: - Prolonged intubation
- After surgeries (abdominal, thoracic, cardiac) - Respiratory acute conditions, exacerbations (asthma, COPD..)
- Neuromuscular diseases
- After extubation
H: Manual techniques : increased expiratory flow, ELTGOL, AD, thoracic + abdominal
compressions, controlled cough
- Instrumental techniques : inhalation therapy, PEP systems, intrapulmonary percussive ventilation IPV, suctioning, MIE
- Association with positioning & NIV - Several times a day
- Protection of surgery scars
D: - Difference between sputum accumulation & acute pulmonary edema
- Difference between intubated & non-intubated patients
- Perform suctioning sparingly
- Valuing interdisciplinary
M: - Vital signs (SaO2, RR, HR, BP)
- Modification of the quality & quantity of sputum - Tiredness, signs of defence
- Breathing pattern
- Dyspnoae
- Auscultation
- Thoracic x-rays (pneumonia, atelectasis)
SUCTIONING: when? Types? Do not forget? Monitoring? How?
W: When patient unable to remove lung secretions - IMV & sedated
- Weak coughing (MEP< 50cmH2O)
- Tracheostomized
- Saw pattern flow volume curve
T: Open circuit
- Decreasing SpO2, Lung collapse? - Infections risk
Closed circuit
D: Training +++
- Assessment mandatory : is this invasive technique most relevant?
- Suctioning must never be systematic - Slow to moderate speed
- Monitoring of risks
M: - Vital signs (SaO2, RR, HR, BP)
- Bronchospasm
- Signs of defense, resistance, pain..
- Color of secretions, especially bloody (technique too agressive or too deep) - Assess efficacy of technique
H: - Hands hygiene at beginning & single-use gloves
- Single-use suction catheter, in its closed package
- Choice of suction catheter size : half of size of intubation catheter - Pre-oxygenation : not mandatory
- Instillation of water : not mandatory, first suction always dry
- Introduction of connected suction catheter using compress
- Lowering of suction catheter : without suction, at moderate speed until stop or cough noticed
- If stop : raise suction probe by about 1cm before suctioning
- Raising suction catheter : continuous suctioning
- Length of suctioning : about 15s
VASODILATORY SHOCK: monitoring & Pathophysiology
Shock & vasopressor therapy
- Characterized physiologically by excessive vasodilation (with low systemic vascular resistance), hypotension & inadequate perfusion (hyperlactatemia, oliguria, confusion)
- Because of inappropriate vascular smooth muscle relaxation as primary event & continued vasodilation despite hypotension, most potent stimulus for vasoconstriction
- Septic shock also often complicated by ventricular dysfunction & hypovolemia in septic shock
Pathophysio
- Adrenergic receptor downregulation, receptor genotype differences between patients, decreased responsiveness in septic shock
- Variable hormone metabolism all conspire to allow continued vasodilation & hypotension
- Profound deficiency of vasopressin later in septic shock
- Major mediators of vasodilation in septic shock = nitric oxide, prostaglandins & NO synthase (iNOS) to simulate NO synthesis
NEUROMUSCULAR ELECTRICAL STIMULATION (NMES): when, how, monitoring, do not forget & contraindications
W: - Intubated patients, mechanical ventilation, sedated or not - ICU-Acquired Weakness (or at risk of)
- Unstable patients
- Stable patients with chronic disease (COPD..)
H: - Start as soon as possible
- Decision taken in agreement with whole ICU team - Check skin of patient ; clean skin if necessary
- Look for motor points of muscles
- Program chosen in order to :
‣ Produce efficient muscle contraction (observable)
‣ Limit pain & discomfort
‣ Minimize fatiguability - At least once day & 5/7 days
M: - Check skin after each session
- Contraction must be visible
- Increase intensity, if well tolerated
D: - Avoid/remove moisturizing creams
- Avoid physical contact between electrods
- Look for motor point on left & on right side (often ≠)
C: - Pacemakers
- Pregnancy
- Venous thrombosis or severe arterial obstruction
- Wounds
- Œdema
- Septic shock
- Patient under vasopressors (noradrenaline, prednisolone..)
O2 THERAPY: def, indications, clinical goal & assessment of need
D: = administration of oxygen at concentrations greater than that in room air to treat or prevent hypoxemia
- Oxygen regarded as drug.
- Oxygen prescribed in all situations (except for immediate management of critical illness in accordance with guidelines) - If abused it can cause complication
I: Hypoxemia – when PaO2 comes down to 60mmHg Normoxic hypoxemia – like low cardiac output state, anemia, CO Poisoning
Trapped gases – like obstruction, pneumocephalus Special situation – like anesthesia
CG: - Treat hypoxemia
- Decrease work of breathing - Decrease myocardial work
AoN: Presence of clinical indicators
Measurement of inadequate oxygen saturation - Arterial blood gas
- Pulse oximetry
‣ Red & infrared light, reflecting on living tissue (Hemoglobin)
‣ To monitor oxyheomoglobin saturation (therapeutic response)
≠ HYPOXEMIA & description of each
HYPOXIC HYPOXEMIA
Causes
- O2 poor air, hypoxic gas mixture
- High altitude
- Hypoventilation
- Shunts (septal defects)
- Diffusion defects (pneumonia, lobar collapses)
ANEMIC HYPOXEMIA
- Oxygen carrying capacity of blood decreased - Anemia
- Altered Hemoglobin: CO Poisoning
STAGNANT HYPOXEMIA
- Inadequate tissue perfusion: - Generalized:
‣ Hypovolemia
‣ Mitral Stenosis
‣ Constrictive pericarditis
‣ Myocardial ischemia
- Localized hypo perfusion:
‣ Arterial obstruction, thrombus, œdema
HISTOTOXIC HYPOXEMIA
- Cells can not utilize oxygen
- Electron transfer system of cytochrome oxidase paralyzed
Example: cyanide poisoning
CLINICAL PRESENTATION OF HYPOXEMIA & BENEFITS OF O2 THERAPY
Acute hypoxia
- Restlessness
- Disorientation
- Confusion
- In-coordination, impaired judgment
- Hyperventilation air hunger
- Circulatory changes (tachycardia → brady)
Chronic hypoxia
- Fatigue
- Drowsiness,
- Inattentiveness
- Apathy
- Delayed reaction time
Tableau
O2 DELIVERY SYSTEM: 2 ≠ types & name & description of each devices
Low flow systems
- Contribute partially to inspired gas client breathes
Ex: nasal cannula, simple mask , non-re breather mask , rebreather mask
High flow systems
- Deliver specific & constant percent of oxygen independent of client’s breathing
Ex: Venturi mask,, trach collar, T-piece
Tableau
O2 THERAPY: evaluation, oxygen flow meter & hazard
E: - Breathing pattern regular & at normal rate
- Pink color in nail beds, lips, conjunctiva of eyes
- No confusion, disorientation, difficulty with cognition - Arterial oxygen concentration or hemoglobin
- Oxygen saturation within normal limits
OF: - Ball must be centered on line
- Diagram illustrates correct setting of flow meter to deliver flow of 2 liters per minute
H: - Drying of mucous membrane
- Depression of ventilation in COPD
- Reversal of compensatory hypoxic vasoconstriction - Atelectasis due to absorption collapse
- O2 toxicity
O2 THERAPY: optimization
My SpO2 is < 90%, what next?
- Is pulse oximeter working/accurate
- Do I have good signal?
- Heart rate plus/minus ?
- Is there adequate perfusion at probe site?
- Can probe be repositioned?
- Do other vital signs or clinical manifestations give evidence of hypoxemia?
Check my source!
- Ensure O2 delivery device attached to oxygen not medical air
- Follow tubing back to source & ensure patency
- Are all connections tight?
Is flows high enough?
- All nebs especially high flow large volume nebs need to be run at highest rate
- Turn flow meter to maximum for large volume nebs
Reposition patient
- Avoid laying patient flat on back
- Raise head of bed
- Encourage deep breathing/coughing
Listen to chest
- Wheezing?
• Do they need bronchodilator?
- Crackles?
• Encourage deep breathing/cough • Are they fluid overloaded?
Can I improve mechanics of breathing? - Patient position
- Pursed lip breathing
- Abdominal breathing
- Anxiety relief?
