Cardiopulmonary Physical Therapy

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Cardiopulmonary Physical Therapy

• Mark Nelson, MPT

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• Objectives for the Module
• Understand the oxygen transport mechanism
• Identify threats to oxygen transport
• Understand cardiopulmonary interventions
• Uderstand how to safely treat the medically
  complex patient

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Pulmonary Function Tests

• Purpose evaluate the mechanical function of the
  lungs
• Based on research norms
• Actual results compared with predicted
• Determines normal function, obstructive or
  restrictive disease

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PFTContinued

• Categorized as
• volume studies
• flow studies
• diffusion studies

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PFTContinued

• Anatomic Dead Space
• conducting airways that do not participate in
  respiration
• grossly proportional to body weight
• sufficient inspired volume to fill dead space and
  provide alveolar ventilation

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PFTContinued

• Anatomic Dead Space
• 150 ml dead space
• normal adult TV 450-600 ml (tidal volume-
  amount of air inhaled and exhaled during normal
  breathing)
• alveolar ventilation 300-450 ml
• dead space is 1/3 of the TV

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PFTContinued

• Anatomic Dead Space
• decreased lobectomy, pneumonectomy, asthma
• increased pulmonary embolism (physiologic dead
  space)

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PFTContinued

• Anatomic Dead Space
• when dead space increases a larger percentage of
  TV ventilates that dead space
• less for alveolar ventilation
• result?
• increased work of breathing

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PFTContinued

• Work of breathing
• minute ventilation (MV)
• MV TV x RR
• 8 L/min 500 ml x 16 bpm
• with exercise or exertion?
• situations that impair MV....

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PFTContinued

• Tidal Volume
• normal breath
• inhalation and exhalation at rest

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PFTContinued

• Inspiratory Reserve Volume (IRV)
• maximum volume inspired above normal inspiration

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PFTContinued

• Expiratory Reserve Volume (ERV)
• amount of volume that can be exhaled after a
  normal exhalation

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PFTContinued

• Reserve Volume (RV)
• volume that remains in the lung at the end of
  maximal expiration

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PFTContinued

• Lung Capacities
• two or more volumes added together
• vital
• functional residual
• total

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PFTContinued

• Vital Capacity (VC)
• maximum volume of air expelled after maximal
  inspiration
• IRVTVREV

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PFTContinued

• Vital Capacity Decrease
• reduction in distensible lung tissue
• restrictive lung disease
• bracing
• neuromuscular dysfunction
• space occupying lesions, body habitus

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PFTContinued

• Vital Capacity Increase
• resolution or improvement of restrive processes
• fixed anatomy and lung volume

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PFTContinued

• Functional Reserve Capacity (FRC)
• volume that remains in the lung at the end of
  normal exhalation
• ERVRV

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PFTContinued

• Functional Reserve Capacity
• prevents large fluctuations in PaO2
• increased value represents hyperinflation of the
  lungs (look for barrel chest, respiratory mm
  inefficiency)
• can be facilitated by mechanical ventilation

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PFTContinued

• Air Flow Measurements
• forced expiration (FEV1)
• the maximal volume of air exhaled in one second
• normal is 75 of vital capacity
• slower with emphysema, dependent on degree of
  disease

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PFTContinued

• Air Flow Measurements
• FEV1 decreases normally 25-30 ml per year
• decline is accelerated for smokers (10-20 ml per
  year greater than non smokers)

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PFTContinued

• Diagnosis of restrictive vs. obstructive
• Restrictive
• conditions that limit the amount of air coming
  into the lungs
• restriction to inspiration

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PFTContinued

• Diagnosis of restrictive vs. obstructive
• Obstructive
• problems with exhalation airflows
• decreased FEV1

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PFTContinued

• Restrictive vs. Obstructive
• patients have components of both

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Oxygen Transport

• Importance cannot be over emphasized
• All patients of physical therapy are
  cardiopulmonary patients on some level
• Need for vigilance and competence
• Maximizing the efficiency of the oxygen transport
  pathway promotes optimal mobility and
  independence, the cornoerstones for quality of
  life and well being

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Oxygen TransportContinued

• Variables
• 1. Oxygen delivery (DO2)
• (arterial oxygen content) x cardiac output
• (oxyhemoglobin) (dissolved oxygen)
• (Hgb x 1.34 x SaO2) (PaO2 x 0.003) x CO

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Oxygen TransportContinued

• Variables
• 2. Oxygen Consumption (VO2)
• (arterial oxygen - venous oxygen) x CO
• (oxyhemoglobin) (dissolved oxygen)
• (Hgb x 1.34 x SvO2) (PvO2 x 0.003) x CO

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Oxygen TransportContinued

• Variables
• 3. Oxygen Extraction Ratio (OER)
• indicates how well oxygen is used at a cellular
  or metabolic level
• OER oxygen consumption / oxygen delivery
• OER VO2 / DO2

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Oxygen TransportContinued

• How is oxygen used?
• cellular metabolism requires a continuous supply
  of ATP, the major source of energy for biological
  work
• contraction of skeletal muscle, smooth muscle and
  for nerve impulse transmission (exercise,
  digestion, glandular secretion, thermoregulation)
• ATP is made primarily by aerobic means

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Oxygen TransportContinued

• How is oxygen used?
• aerobic metabolism occurs in the mitochondria via
  the Krebs cycle and electron transfer chain
• oxygen is harnessed for oxidative reactions and
  as an electron receptor in the production of
  water
• for each molecule of glucose that is metabolized
  36 molecules of ATP are produced

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Oxygen TransportContinued

• How is oxygen used?
• 32 molecules via oxidative phosphorylation
  (the aerobic pathway)
• 4 molecules via substrate phosphorylation
  (the anaerobic pathway)
• low ATP yield
• short term energy production
• inefficiency
• disruptive effects of lactate

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Oxygen TransportContinued

• How is oxygen used?
• normally oxygen delivery is regulated by tissue
  metabolism as well as the overall demand for
  oxygen
• at rest DO2 is 3-4 times greater than VO2
• in healthy people, exercise is the greatest
  challenge to oxygen transport system
• VO2 can increase as much as 20 times resting in
  response to increased muscle metabolism
• cardiac function increases based on workload

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Normal Heart Rate Response with Exercise
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Normal Time to Steady State Heart Rate
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Normal Stroke Volume Response with Exercise
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Normal Cardiac Output Response with Exercise
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Normal Pressure Response with Exercise
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Oxygen TransportContinued

• Preferential Distribution of CO
• rest
• 20 kidneys
• 20-30 to gut, spleen, liver
• 10 muscle
• 5 each brain and myocardium
• Guyton, AC et al (2000). Textbook of medical
  physiology, ed. 10. Philadelphia Elesevier

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Oxygen TransportContinued

• Preferential Distribution of CO
• 
  

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Oxygen TransportContinued

• Management of Oxygen
• rightward shift of oxyhemoglobin dissociation
  curve (increased heat and lowered pH)
• results in lower binding of oxygen to hemoglobin
• cessation of exercise results in leftward shift
  back to baseline
• increased metabolic demand causes increased
  capillary dilation, reduced vascular resistance
  to flow, decreased diffusion distance

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Oxygen TransportContinued

• Management of Oxygen
• oxygen extraction ratio is that amount of oxygen
  consumed
• VO2 / DO2
• at rest OER 23
• those who are critically ill may not have
  sufficient DO2 to meet basic metabolic needs (300
  ml/min/m2)
• decreased DO2 leads to lactic acidosis and
  falling pH

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Oxygen TransportContinued

• Quantity and Quality of Blood
• blood must delivered at varying amounts based
  metabolic demand
• blood is compartmentalized
• 70 within the venous space
• 10 in systemic arteries
• 15 in systemic circulation
• 5 in capillaries
• Sandler, H Cardiovascular Effects of Inactivity.
  In Sandler, H Vernikos, J (eds). Inactivity
  Physiological Effects. Orlando Academic Press
  1986.

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Oxygen TransportContinued

• Quantity and Quality of Blood
• this allows for easy manipulation of CO as veins
  constrict
• compartmentalization relies on normal fluid
  distribution
• when blood volume is abnormal, body fluids can
  become inappropriately distributed between
  extracellular and intravascular spaces
• changes electrolyte concentration, particularly
  sodium

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Oxygen TransportContinued

• Quantity and Quality of Blood
• proper hematocrit (Hct) proper number of RBCs
• blood is viscous
• normals
• men 42
• women 38
• polycythemic
• viscosity increases greatest effect on the
  smaller vessels, increasing friction, decreasing
  flow- stuck

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Oxygen TransportContinued

• Quantity and Quality of Blood
• proper hematocrit (Hct) proper number of RBCs

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Oxygen TransportContinued

• Quantity and Quality of Blood
• proper resident chemistry to keep platelets
  inactivated (prostacyclin and thromboxane)
• preventing aggregation and adherence which begins
  the clotting cascade

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Oxygen TransportContinued

• Steps in the Oxygen Transport Pathway
• 1. Inspired oxygen and quality of ambient air
• room air 21 O2
• room air 79 N2
• nitrogen helps keep alveoli open (inert gas)
• exposure to hazardous gases
• production of sputum can overwhelm cilia
• dehydration of mucus membranes, upper respiratory
  tract -- source of infection

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Oxygen TransportContinued

• Steps in the Oxygen Transport Pathway
• 2. Airways
• differences in structure and types of tissue,
  from trachea to alveolus
• cilia
• obstruction of various kinds

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Oxygen TransportContinued

• Steps in the Oxygen Transport Pathway
• 3. Lungs and chest wall
• integrity of respiratory muscles
• diaphragm excursion
• ability to create and maintain negative pressure
• act of breathing helps to pump lymph from the
  peritoneal cavity to the thoracic duct
• if lymph flow backs up in the abdomen this leads
  to accumulation of high protein content fluid in
  the abdomen -- ascites

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Oxygen TransportContinued

• Ascites

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Oxygen TransportContinued

• Steps in the Oxygen Transport Pathway
• 4. Diffusion of gases
• capillary membrane area
• diffusing capacity of the capillary membrane
• pulmonary capillary blood volume
• ventilation / perfusion ratio
• blood remains in the pulmonary capillaries 0.75
  seconds, saturates in 0.25 seconds

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Oxygen TransportContinued

• Steps in the Oxygen Transport Pathway
• 5. Perfusion
• distribution is primarily gravity dependent
• dependent lung fields are better perfused than
  the nondependent fields
• upright lungs -- bases better than apices
• ventilation and perfusion matching are best in
  the midzones (normal ratio is 0.8)

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Oxygen TransportContinued

• Steps in the Oxygen Transport Pathway
• 6. Myocardial function
• CO 4-6 L/min
• CI 2.5-4.5 L/min/m2
• proper preload
• adequate contractility
• EF sufficient to overcome vascular resistance in
  pulmonary and peripheral vasculature (afterload)

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Oxygen TransportContinued

• Steps in the Oxygen Transport Pathway
• 7. Peripheral circulation
• proper vasculature
• maintenance of smooth muscle tone and sufficient
  response to gravity challenge
• moment to moment regulation by neural and humoral
  stimulation
• maintenance of pressure gradient at the capillary
  (0.3 mm Hg) to the interstitial space

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Oxygen TransportContinued

• Steps in the Oxygen Transport Pathway
• 8. Tissue extraction and utilization of oxygen
• diffusion occurs along a gradient
• intracellular PaO2 ranges 5-60 mm Hg with an
  average of 23 mm Hg
• PaO2(crit) 3 mm HG (minimum required to support
  metabolism)
• normal rate of extraction is governed by O2
  demand of cells and not by supply

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Oxygen TransportContinued

• Steps in the Oxygen Transport Pathway
• 9. Return of partially desaturated blood and CO2
  to the lungs
• alveolar ventilation (depth and rate of
  breathing)
• competent venous circulation
• carbonic anhydrase -- facilitates the
  carboxyhemoglobin loading reaction catalyzes the
  reaction between CO2 and H2O

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Oxygen TransportContinued

• Normal Challenges to Oxygen Transport
• 1. Gravitational stress
• changes in body position have significant effect
  on the distribution of fluids
• 60 of body weight is fluid
• contained in the intravascular and extracellular
  spaces
• change in body position fluid shifts
• impaired by prolonged recumbency
• primary cause of bed rest deconditioning

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Oxygen TransportContinued

• Normal Challenges to Oxygen Transport
• 1. Gravitational stress
• fluid shifts cause symptoms along a continuum
• asymptomatic
• mild, short lived light headedness
• pre-syncope
• syncope
• seizure
• reorientation to gravity os the only method of
  training the cardiovascular system

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Oxygen TransportContinued

• Normal Challenges to Oxygen Transport
• 2. Exercise stress
• greatest perturbation to homeostasis and oxygen
  transport
• best effect is combine gravitational stress with
  exercise stress

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Oxygen TransportContinued

• Normal Challenges to Oxygen Transport
• 3. Emotional stress
• anxiety, fear, agitation, perceived threat
• primes the fight or flight response and increases
  sympathetic nervous system stimulation

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Diagnosis Challengescontinued

• Acute Respiratory Distress Syndrome

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Diagnosis Challengescontinued

• Acute Respiratory Distress Syndrome
  (Hansen-Flaschen)
• Severe lung injury characterized by
• inflammatory injury to alveoli
• normal barriers to alveolar edema are lost,
  protein escapes from the vascular space and
  osmotic gradient favoring resorption of fluid is
  lost
• fluid pours into the interstitium and overwhelms
  the lymphatic system
• air spaces fill with bloody proteinaceous edema
  fluid and debris from degenerating cells

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Diagnosis Challengescontinued

• Acute Respiratory Distress Syndrome
• Progression
• injury (direct or indirect)
• initiation of inflammatory-immune response
• activation of neutrophils and macrophages
• release of endotoxin
• release of mediators
• increased capillary permeability, changes in
  small airway diameter, injury to pulmonary
  vasculature, pulmonary hypertension, alveolar
  collapse, hypoxia

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Diagnosis Challengescontinued

• Acute Respiratory Distress Syndrome (cont.)
  (Hansen-Flaschen)
• Impaired gas exchange
• ventilation/perfusion mismatch
• physiologic shunting
• increased physiologic dead space
• decreased CO2 elimination
• hypoxia

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Diagnosis Challengescontinued

• Acute Respiratory Distress Syndrome (cont.)
  (Hansen-Flaschen)
• Decreased lung compliance
• increased stiffness of poorly or nonaerated lung
• decreased ventilation
• Pulmonary hypertension

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Diagnosis Challengescontinued

• Acute Respiratory Distress Syndrome (cont.)
  (Hansen-Flaschen)
• Treatment
• DVT prophylaxis
• treatment of nosocomial pneumonia
• nutritional support
• mechanical ventilation with aggressive sedation
  and analgesia
• supplemental oxygen
• prone position, rotation and percussion

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Diagnosis Challengescontinued

• Deep Vein Thrombosis

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• 2 million cases reported each year in US
• 600,000 (30) lead to pulmonary embolism
• 60,000 (10) of incidences of PE lead to death
• DVT can be an acute or chronic condition
• sequela of immobilization, surgery, cancer
• hypercoagulable states

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Deep Veins
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Deep Veins
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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Venous thrombi are an accumulation of platelets,
  the fibrin mesh they produce and primarily RBCs

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Diagnosis Challengescontinued

• Deep Vein Thrombosis

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Venous thrombi are an accumulation of platelets,
  the fibrin mesh they produce and primarily RBCs
• Thrombosis occurs when certain conditions exist
• tissue damage (releases factors activating
  platelets)
• when activated, platelets form fibrin mesh that
  trap cellular components of blood, slows flow of
  plasma

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Thrombosis occurs when certain conditions exist
• tissue damage
• activated platelets demonstrate
• adherence- attachment to endothelium or exposed
  collagen
• aggregation- attachment to other activated
  platelets

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Diagnosis Challengescontinued

• Deep Vein Thrombosis

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Thrombosis occurs when certain conditions exist
• tissue damage
• fall, fracture, trauma
• surgery
• cancer

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Thrombosis occurs when certain conditions exist
• venous stasis
• prevents clearance of mediators of inflammation
  and activated coagulation factors
• reduces flow of agents that deactivate clotting
• reduces flow of phagocytes
• allow adherence and aggregation to occur with
  greater ease

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Thrombosis occurs when certain conditions exist
• venous stasis
• immobilization (for any reason, but esp. after
  surgery)
• decreased cardiac output (CHF, MI, decreased EF)
• decreased skeletal mm activity (CVA)
• venous occlusion (sitting postures, compression)

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Thrombosis occurs when certain conditions exist
• vascular injury
• damage to veins or endothelial tissue
• inflammatory response
• imbalance in resident chemistry that keeps
  platelet function in check (prostacyclin and
  thromboxane)

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Thrombosis occurs when certain conditions exist
• vascular injury
• intra-operative damage
• cannulation (IVs, catheterization)
• previous DVT
• post-operative sepsis

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Superficial vein thromboses are usually well
  isolated and self limiting (e.g. varicose veins)
• SVT rarely extend into the deeper veins
• DVTs in distal circulation are generally less
  dangerous than more proximal DVTs
• usually smaller and self limiting
• dont have the same clinical, symptomatic or
  occlusive impact

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Symptoms occur as a result of size and location
• obstructing venous outflow
• edema
• tenderness/ pain
• cause inflammation of the vein wall
• edema
• tenderness/ pain
• embolize and travel to the lungs (PE)
• tachycardia, pulm. HTN, dyspnea, resp. failure

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Diagnosis Challengescontinued

• Deep Vein Thrombosis

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Strong correlation between DVT and PE
• PE are detected in 50 of patients with
  documented DVT
• asymptomatic venous thrombosis is found in 70
  of patients with clinically symptomatic PE
• When embolization of a small thrombus occurs, the
  clinical impact is usually small (single
  incident)
• Shower emboli can overload the pulmonary
  circulation and lead to right heart failure

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Thrombi that arise from proximal veins and are
  large will be symptomatic, potentially fatal.
• Occlusion at or above the popliteal vein is
  considered proximal
• Deep calf vein thrombosis is considered distal

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Diagnosis
• clinical signs and symptoms of DVT are not
  sensitive or specific
• DVT present DVT
  absent
• Pain 78
  75
• Edema 78
  67
• Homans Sign () 56
  61
• ODonnell T, Abott W, Anthanasoulis C, Millan V,
  Callow A. Diagnosis of proximal deep venous
  thrombosis. Ir Med J 1982 75119-120

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Diagnosis
• other causes of LE pain that mimic DVT
• SVT
• cellulitis
• trauma
• vasculitis
• lymphedema

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Diagnosis
• consider risk factors
• age gt60 yrs
• extensive surgery
• previous DVT
• major orthopedic surgery
• fracture of pelvis, femur, tibia
• sepsis
• cancer

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Diagnosis
• objective tests that are not imaging, have
  sensitivity approaching 50 (Homans sign,
  palpation)
• definitive diagnosis made by imaging
• 1. Venography
• 2. Impedance plethysmography
• 3. Venous ultrasound

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Diagnosis
• 1. Venography
• radiographic material is injected into a
  superficial vein in the foot and mixes with
  venous blood
• venous blood flows proximally
• x-ray taken visualizing the leg and pelvis
• venous thrombosis confirmed by filling defect
  in the lumen of a vein.

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Diagnosis
• 2. Impedance plethysmography
• electrodes are attached to the calf and a blood
  pressure cuff placed around the thigh
• differences in impedance are recorded when blood
  volume changes in response to cuff pressure
• looks at the amount of time it takes for venous
  flow to return to baseline after compression
• slower venous emptying is positive for DVT

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Diagnosis
• 3. Venous ultrasound
• creates two dimensional image by computation of
  reflected signals from an array of ultrasound
  sources
• veins are visualized, and then gently compressed
  with the sound head
• thrombotic vessels are non compressible

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Treatment
• prevent extension of the existing clot
  (anticoagulation)
• prevent portions of the clot from breaking free
  (embolization)
• aid thrombolysis when appropriate

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Treatment
• anticoagulation
• heparin begins to work immediately upon
  administration by inhibiting activated clotting
  factors
• coumadin works more slowly by inhibiting
  synthesis of vitamin K dependent coagulation
  proteins
• does nothing to reduce the existing clot,
  only prevents further clot from forming

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Treatment
• prevent embolization
• greatest risk of clot mobilization occurs in
  acute phase
• clot is least organized, least adhered most
  unstable
• allow time for anticoagulation therapy to work
  (reduce or stop the formation of additional clot)
• allow time for clot to organize

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Treatment
• prevent embolization
• insertion of filters in the vena cava to ensnare
  wayward thrombus before reaching pulmonary
  circulation (TrapEase, Greenfield, Birds Nest)
• indicated in patients who cannot tolerate chronic
  anticoagulation or with recurrent thromboembolism

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• Inferior Vena Cava Filters

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Treatment
• thrombolysis
• streptokinase and tPA
• thrombolytic agents convert plasminogen to
  plasmin (an enzyme that dissolves fibrin)
• thrombolysis is indicated for massive iliofemoral
  DVT and PE with hemodynamic instability
• bleeding and intracranial hemorrhage are risks

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Treatment
• resumption of PT
• when is it safe to ambulate or exercise?
• 5 MDs, 5 answers (no hard and fast rules)
• SVT vs DVT, distal vs proximal, UE vs LE
• PTT 42-55 sec (low therapeutic range) x 24 hours
• PTT 42-72 high (high therapeutic range) x 24 hours

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Treatment
• resumption of PT
• Bed Rest or Ambulation in the initial Treatment
  of Patients with Acute Deep Vein Thrombosis or
  Pulmonary Embolism Santos et al, Chest 2005
  127 1631-1636
• 2650 patients in the study (2038 with DVT 612
  with PE)

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Treatment
• resumption of PT
• Santos et al, Chest 2005 127 1631-1636
• 1050 DVT (52) and 385 PE (63) pts were
  prescribed strict bed rest
• new events of symptomatic, objectively confirmed
  PE developed during the 15-day study in 11 pts
  with DVT (0.5) and 4 pts with PE (0.7)

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Treatment
• resumption of PT
• Santos et al, Chest 2005 127 1631-1636
• there are no differences in the rate of new PE
  episodes between patients who have been
  immobilized in bed and those who are allowed to
  walk

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Treatment
• resumption of PT
• Santos et al, Chest 2005 127 1631-1636
• our study confirms that symptomatic PE events
  occurring during the first 2 weeks of therapy in
  patients with either acute DVT or PE are
  infrequent, however, when they do occur they are
  extremely serious
• five of the 15 who developed new PE died (33)

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Treatment
• resumption of PT
• Santos et al, Chest 2005 127 1631-1636
• weaknesses, not a RCT
• selection process (ambulatory vs non ambulatory
  groups) ambulation may have been prescribed to
  healthier patient
• no evaluation of asymptomatic recurrences

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Treatment
• resumption of PT
• Santos et al, Chest 2005 127 1631-1636
• ...there were not significant differences
  between bed ridden and ambulant patients in terms
  of new PE events, fatal PE or bleeding
  complications.

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Treatment
• resumption of PT
• when is it safe to ambulate or exercise?
• PT/INR 1.5-3.0 for at least 72 hours
• no obvious evidence of trailing tail on doppler
  or CT (high risk of embolization)

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Outcomes
• thrombus extends
• clot creates its own micro-environment (clotting
  factors, inflammatory process, venous stasis)
• clot can grow either proximal or distal to
  original clot site
• thrombus resolves
• autolytic process dissolves the clot,
  resolution, little damage

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Outcomes
• organization
• occurs with phagocytosis and scar tissue is
  formed within the clot matrix (increases
  adherence to vein wall, increases stability)
• further organization of the clot
• includes recanalization of the occlusive clot
  (holes eaten into clot, then relined with
  epithelial tissue)
• reduces vessel lumen and venous function

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Outcomes
• many patients recover completely
• two long term complications
• 1. post thrombotic syndrome
• leg pain, edema, venous hypertension,
  venous insufficiency, ulceration
• 30 of patients with DVT develop post thrombotic
  syndrome
• (Prandoni P et al. The long term clinical course
  of acute deep venous thrombosis.
  Ann Intern Med 19961251-7)

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Outcomes
• two common long term complications
• 2. chronic thromboembolic hypertension
• pulmonary hypertension caused by incomplete
  resolution of clot in the lung circulation
• limited by progressive exertional dyspnea, chest
  pain, syncope
• seen in up to 5 of patients
• (Rubiero A et al Pulmonary embolism one year
  follow up with echocardiography doppler and five
  year survival analysis. Circulation.
  1999991325-1330)

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Prophylaxis
• preventing or interrupting the activation of
  blood coagulation (aggregation and adherence)
• low dose subcutaneous heparin
• oral anticoagulants
• LMWH
• preventing venous stasis
• intermittent pneumatic compression of the legs
• graduated compression stockings

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• Prophylaxis
• preventing venous stasis (cont.)
• teach importance of muscle pump action
• mobilize, ambulate

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Diagnosis Challengescontinued

• Deep Vein Thrombosis
• When in doubt confer with MD or nurse about the
  relative risk of your intervention
• If you cant find evidence of anticoagulation,
  defer therapy
• Look for indications of instability
• Assess, assess, assess!!

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Diagnosis Challengescontinued

• Pulmonary Embolism

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Diagnosis Challengescontinued

• Pulmonary embolism (Thompson)
• Approximately 500,000 diagnoses of PE are made
  annually
• Nearly 200,000 result in death
• Estimated that half of all patients with PE
  remain undiagnosed
• Usually arise from thrombi originating from the
  deep venous system in the lower extremities

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Diagnosis Challengescontinued

• Pulmonary embolism (cont.)
• Embolic thrombus travels proximally
• through venous system
• into the IVC
• into the right atrium
• right ventricle
• pulmonary artery
• Endpoint depends on size of thrombus/vessel size
  relationship and/or vessel path

118
Diagnosis Challengescontinued

• Pulmonary embolism (cont.) (Thompson)
• After traveling to the lung, large thrombi may
  lodge in the bifurcation of the main pulmonary
  artery and cause hemodynamic compromise
• Smaller thrombi continue traveling distally and
  are more likely to cause pleuritic chest pain
• Most PE are multiple, affecting primarily the
  lower lobes
• Approximately 10 of thrombi will cause pulmonary
  infarction

119
Diagnosis Challengescontinued

• Pulmonary embolism (cont.)
• Larger thrombus can block bifurcation of
  pulmonary artery, right and left main pulmonary
  arteries
• Diminishing or blocking supply of blood to both
  lungs Saddle Embolus
• Resultant ischemia, infarct and death

120
Diagnosis Challengescontinued

• Pulmonary embolism (cont.)

121
Diagnosis Challengescontinued

• Pulmonary embolism (cont.) (Thompson)
• Risk factors
• immobilization
• surgery within the last three months
• stroke
• history of venous embolism

122
Diagnosis Challengescontinued

• Pulmonary embolism (cont.) (Thompson)
• Symptoms
• may be asymptomatic
• dyspnea
• tachypnea
• pleuritic pain, diffuse chest pain
• persistent cough
• tachycardia or arrhythmia
• hemoptysis
• fever

123
Diagnosis Challengescontinued

• Pulmonary embolism (cont.) (Thompson)
• Symptoms
• like DVT symptoms, PE can be non specific
• similar symptoms from other sources
• pulmonary infection
• COPD exacerbation
• atelectasis

124
Diagnosis Challengescontinued

• Pulmonary embolism (cont.) (Thompson)
• Diagnosis
• most reliable test is pulmonary angiography
• looks for intraluminal filling defect in
  pulmonary circulation
• ventilation/perfusion study
• looks for normal ventilation with impaired
  perfusion (normal scan excludes dx of PE)

125
Diagnosis Challengescontinued

• Pulmonary embolism (cont.) (Thompson)
• Treatment
• anticoagulation with heparin followed by coumadin
• thrombolytic therapy
• oxygen and supportive therapy
• vena cava filter placement for recurrent PE
• Resumption of therapy as per DVT
• monitor closely for changes in saturation, HR and
  subjective symptomology

126
Treatment

• Cardiopulmonary aspects of acute care therapy
• Treatment needs to match the underlying
  pathophysiology- identify the problem
• Form a problem list regarding impaired oxygen
  transport
• functional aspects (limitations in ADLs,
  deconditioning)
• physiologic (deficits in cardiovascular or
  pulmonary function)

127
Treatmentcontinued

• Deficits
• neurological control
• altered CNS control of breathing
• pharmacologic depression
• airway
• aspiration
• obstruction
• lungs
• lung compliance
• diaphragm function
• pulmonary toilet and secretion management

128
Treatmentcontinued

• Deficits (contd)
• lungs
• loss of normal chest wall movement
• chest wall/spinal column deformities
• acute injury (ARDS, sepsis)
• blood
• bleeding
• hypo/hyperthermia
• low Hct/Hgb
• abnormal clotting DIC

129
Treatmentcontinued

• Deficits (contd)
• gas exchange
• alveolar collapse
• atelectasis
• mucus
• pulmonary edema
• ventilation perfusion mismatch
• pleural effusion
• pulmonary emboli
• diffusion defects due to gas gradients

130
Treatmentcontinued

• Deficits (contd)
• respiratory muscles
• abdominal surgery
• ileus
• deconditioning
• fatigue
• mechanical or neurological dysfunction
• myocardial perfusion
• CAD
• tachycardia

131
Treatmentcontinued

• Deficits (contd)
• heart
• decreased venous return (preload)
• conduction defects
• altered total peripheral resistance (afterload)
• mechanical defects (valvular, inotropic)
• decreased CO
• blood pressure
• hypovolemia/bleeding
• altered distribution/shunting

132
Treatmentcontinued

• Deficits (contd)
• tissue perfusion
• decreased CO
• microvascular thrombi
• hypovolemia
• atherosclerosis, thromboembolism
• decreased vascular integrity
• low oxygen saturation
• tissue oxygenation
• altered gas exchange at the cellular level

133
Treatmentcontinued

• Deficits (contd)
• fluid volume excess
• aggressive IV administration
• impaired excretion/ renal insufficiency
• hemodynamic instability from bed rest, edema
• sodium retention
• increased levels of aldosterone, renin,
  angiotensin

134
Treatmentcontinued

• Deficits (contd)
• fluid volume deficit
• insufficient oral intake
• blood loss (internal injury, surgical fluid loss)
• vomiting, diarrhea
• NG suctioning
• sepsis, shock
• burns

135
Interventions

• Wake Forest Study shows early and progressive PT
  decreases LOS in ventilated respiratory failure
  patients (in publication, press release, Wake
  Forest website 10/23/07)
• http//www1.wfubmc.edu/News/NewsARticle.ht
  m?ArticleID2182
• PHYSICAL THERAPY IN ICU REDUCES HOSPITAL
  STAYS, STUDY SHOWS
• http//www.apta.org/AM/Template.cfm?SectionArchiv
  es2TEMPLATE/CM/ContentDisplay.cfmCONTENTID4428
  7

136
InterventionsContinued

• Mobilization and Exercise
• Mobilization
• therapeutic and prescriptive application of low
  intensity exercise in the management of cardiac
  and pulmonary disfunction, usually in patients
  who are acutely ill
• involves position change of the body to exploit
  gravitational stress

137
InterventionsContinued

• Mobilization and Exercise
• Exercise
• therapeutic and prescriptive exertion to
  challenge the oxygen transport mechanism
• exploit the cumulative and adaptive effects
  (training response)
• progressive vs. maintenance

138
InterventionsContinued

• Physiologic goals of therapy intervention
• 1. Short term
• correct or reverse cardiopulmonary dysfunction
• reduce rate of deterioration
• avoid worsening patients condition

139
InterventionsContinued

• Physiologic goals of therapy intervention
• 2. Long term
• enhance efficiency of the steps in oxygen
  transport
• enhance efficiency of compensations to acute and
  chronic disease
• optimize oxygen transport capacity to sustain
  maximal functional activity

140
InterventionsContinued

• Physiologic goals of therapy intervention
• 3. Prevention
• prevent further cardiopulmonary dysfunction
• preserve multisystem organ function
• prevent further restricted movement
• patient education in importance of movement and
  safe mobility

141
InterventionsContinued

• Acute physiologic effects
• pulmonary system
• ?pulmonary function
• ?regional ventilation
• ?regional perfusion
• ?tidal volume
• ?minute ventilation (TVxbpm)
• ?respiratory mechanics efficiency
• ?cough efficiency
• ?distribution and function of pulmonary immune
  factors

142
InterventionsContinued

• Acute physiologic effects
• cardiovascular system
• ?venous return
• ?stroke volume
• ?heart rate
• ?CO
• ?coronary perfusion
• ?total peripheral resistance
• ?peripheral blood flow
• ?peripheral tissue oxygenation

143
InterventionsContinued

• Acute physiologic effects
• lymphatic system
• ?pulmonary lymphatic flow
• ?pulmonary lymphatic drainage
• hematologic system
• ?blood flow velocities
• ?blood stasis
• ?risk of DVT

144
InterventionsContinued

• Acute physiologic effects
• neurological system
• ?LOC
• ?cerebral electrical activity
• ?stimulus to breathe
• ?sympathetic stimulation
• ?postural reflexes
• urinary system
• ?glomerular filtration
• ?urinary output

145
InterventionsContinued

• Acute physiologic effects
• gastrointestinal system
• ?gut motility
• ?constipation
• multisystemic effects
• ?effects of anesthesia and sedation
• ?loss of gravitational stimulus
• ?in mood

146
InterventionsContinued

• Therapeutic effect is proportional to time
  between treatment interventions
• teach patient to carry out prescriptive treatment
  on a schedule or when ever possible, include
  patients family and NSG
• homework assignments

147
InterventionsContinued

• Mobilization (therapeutic and prescriptive
  application of low intensity activity) and
  exercise
• Create an environment where the patient can exert
  such that they raise the demand for oxygen and
  blood flow the acute effects of exercise to
  optimize cardiopulmonary function
• Performed in an upright position to facilitate
  central and peripheral hemodynamics, fluid
  shifts, postural challenge and exercise strain

148
InterventionsContinued

• Mobilization and exercise prescription is not
  well studied in the literature
• Even for critically ill patients the goal is to
  evaluate their oxygen transport reserve capacity
• Estimate the limits of a patients physiologic
  tolerance for mobilization or exercise
• Continuum
• dangling at EOB
• Bruce protocol

149
InterventionsContinued

• Prescription of mobilization and therapeutic
  exercise is neglected in the research
• how much, how often, how intense?
• Exercise testing and the acute care patient?
• cant be done in the standard manner
• imperative that the therapist can identify
  specific effects of mobilization and exercise,
  define optimal therapeutic stimulus
• maximize benefit while decreasing risk

150
InterventionsContinued

• In acute illness, the patient spends a great deal
  more time recumbent and not moving than a person
  dealing with chronic disease
• Made worse by limited prior level of function,
  obesity, smokers, older people, mechanical
  ventilation
• Inactive or sedentary individual
• Community dweller
• Active exerciser
• Competitive athlete

151
InterventionsContinued

• The goal is to correct the deconditioning and
  loss of normal gravitational stress response

152
InterventionsContinued

• Metabolic demand of acute patients is different
  than for healthy persons
• basal metabolic rate
• other demands
• increased body temp
• healing and repair (anabolism)
• increased work of breathing
• pain, anxiety, response to PT
• response will be altered depending on extent and
  severity of cardiopulmonary disease

153
InterventionsContinued

• Metabolic demand of acute patients is different
  than for healthy persons
• a relationship between DO2 and VO2 must be made
  during assessment
• can the system support metabolic needs?
• what reserve capacity is available to support
  mobilization or exercise stimulus?
• consider undue oxygen demand and therapy
  techniques for relaxation and calming

154
InterventionsContinued

• Mobilization and exercise prescription utilizes
  ACSM concepts
• 1. type of mobilization or exercise (mode)
• 2. specific intensity (Borg scale of RPE)
• 3. duration
• 4. frequency
• ACSM Guidelines for Exercise Testing and
  Prescription, ed 6. Philadelphia Williams and
  Wilkins 2000.
• (5). course of prescription (time RX will provide
  maximum benefit
• (6). progression

155
InterventionsContinued

• Mobilization and exercise prescription
• 1. Identify all factors contributing to deficits
  in oxygen transport
• 2. Determine whether mobilization and exercise
  are indicated, and how they affect factors in
  step 1
• 3. Match appropriate mobilization or exercise
  stimulus to the patients oxygen transport
  capacity
• 4. Set the intensity with in therapeutic and safe
  limits, monitor for change

156
InterventionsContinued

• Mobilization and exercise prescription
• 5. Combine various body positions with
  progressively more challenging activities
• 6. Set the duration of the mobilization sessions
  according to patient responses rather than time
• 7. Repeat mobilization sessions as often as
  possible according to their beneficial effects

157
InterventionsContinued

• Mobilization and exercise prescription
• 8. Increase the intensity of the mobilization
  stimulus, the duration or both, monitoring
  responses to activity
• 9. Progress the program until
• functional status allows resumption of activities
  and full participation in life
• the threat to oxygen transport is minimized

158
InterventionsContinued

• Mobilization and exercise prescription
• Monitoring the patient
• HR
• ECG
• BP
• rate-pressure product (HR X SBP)
• RR
• SpO2

159
InterventionsContinued

• Mobilization and exercise prescription
• Monitoring the patient
• rating of perceived exertion
• rating of perceived dyspnea
• pain

160
InterventionsContinued

• Mobilization and exercise prescription
• Safety with critically ill patients
• review medical background
• sufficient cardiovascular reserve?
• sufficient respiratory reserve?
• PaO2/FIO2 gt 300
• all other factors favourable
• Stiller, K Safety Issues That Should be
  Considered when Mobilizing Critically Ill
  Patients. Critical Care Clinics. 2007 235-53.

161
InterventionsContinued

• Mobilization and exercise prescription
• Is the patient tolerating what your intervention?
• appropriate incremental increase in HR
• rise in SBP
• stable or small rise in DBP
• sinus rhythm (no change in underlying rhythm)
• PaO2/FIO2 stable
• lt4 decrease in SpO2
• patient appears unstressed
• Stiller, K Safety Issues That Should be
  Considered when Mobilizing Critically Ill
  Patients. Critical Care Clinics. 2007 235-53.

162
InterventionsContinued

• Mobilization and exercise prescription
• Monitoring the patient -- when to stop
• wish of the individual for any reason
• failure of monitoring equipment
• fatigue
• dizziness, confusion, ataxia, pallor, cyanosis,
  dyspnea, nausea, onset of angina
• ACSM Guidelines for Exercise Testing and
  Prescription, ed 6. Philadelphia Williams and