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Slide 1
I Found the Vital Sign: Now What? Demystifying What All Those Numbers
Mean for Complex Patient ManagementJ. Dyson, Orlando Health, Orlando, FL
K. Levenhagen, Saint Louis University, Saint Louis, MO
T. Norris, Barnes-Jewish Hospital, Saint Louis, MO
K. Swanick, Florida Gulf Coast University, Fort Meyers, FL
J. Tompkins, Mayo Clinic, Phoenix, AZ
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Slide 2 Objectives
• By the end of the presentation, the learner will:• Recognize the importance of determining vital signs prior to initiating an
examination/intervention.
• Describe the clinical considerations related to abnormal physiological and hemodynamic indicators.
• Classify vital signs that are pertinent to physical therapy professionals and their implications on the movement system.
• Utilize the various invasive and noninvasive measures to appropriately dose intervention and identify absolute parameters for therapeutic participation.
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Slide 3 What are vital signs?
• Merriam Webster: important body functions (such as breathing and heartbeat) that are measured to see if someone is alive or healthy• Clinical decision making
• Body temperature
• Heart rate
• Breathing rate
• Blood pressure
• Pulse oximetry
• Pain
• Walking speed
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Slide 4 So why are we not taking vitals?
Thistle et al (2016)
Vitals % of Outpatient PTs
BP 41%
HR 35.3%
RR 17.6%
Pulse Oximetry 29.4%
Temp 5.9%
Frese et al (2002)
Facility HR/BP Never or < half the time
HR/BP Always or > half the time
Acute Care 76.8%/83.9% 23.2%/16.1%
Rehabilitation 70.9%/69.1% 29.1%/30.9%
Extended Care Facility 53.8%/61.5% 46.2%/38.5%
Home Health 11.1%/22.2% 88.9%/77.8%
Outpatient 91.5%/92.1% 8.5%/7.9%
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Slide 5 So why are we not taking vitals?
• Patient young in age
• Previously documented by health care professional
• No documented history of cardiovascular comorbidities
• Taking blood pressure medication
• Time constraints
• Implementation
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Slide 6 Why should you take vital signs?
• 62% of OP PT orthopedic patients have secondary cardiovascular disease Billek-Sawhney, 1998
• Increased energy expenditure Schmalz, 2002• 20-40% transtibial amputee ambulation• 50-80% transfemoral amputee ambulation• 300% bilateral transfemoral
• Interpreting cardiovascular response is multifactorial• Risk factors/PMH• Type and dosage level of cardiac meds• Vitals signs (before, during, and after)• Patient report• Your observations
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Slide 7 Movement System (APTA 2017)
• PTs provide a unique perspective on purposeful, precise, and efficient movement across the lifespan based upon the synthesis of their distinctive knowledge of the movement system and expertise in mobility and locomotion.
• PTs examine and evaluate the movement system (including diagnosis and prognosis) to provide a customized and integrated plan of care to achieve the individual's goal-directed outcomes.
• PTs maximize an individual's ability to engage with and respond to his or her environment using movement-related interventions to optimize functional capacity and performance.
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Slide 8 Systemic Blood Flow at Rest and Exercise Healthy Young Individual
OrganResting(mL/min)
Mild exercise(mL/min)
Maximal exercise(mL/min)
Skeletal muscle 1200 4500 12,500
Heart 250 350 750
Brain 750 750 750
Integument 500 1500 1900
Kidney 1100 900 600
Gastrointestinal 1400 1100 600
Others (i.e., liver, spleen)
600 400 400
Total 5800 9500 17,500
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Slide 9
DigestiveAbsorbs nutrients and water; delivers nutrients to liver for processing by hepatic portal vein; provides nutrients essential for hematopoiesis and building hemoglobin
EndocrineDelivers hormones: atrial natriuretic hormone (peptide) secreted by the heart atrial cells to help regulate blood volumes and pressures.
IntegumentCarries clotting factors, platelets, and white blood cells for homeostasis, fighting infection and repairing damage; regulates temperature by controlling blood flow to the surface.
LymphaticTransports white blood cells and antibodies throughout the body to maintain health; carries excess tissue fluid not reabsorbed by the vascular capillaries.
Muscular Removes lactic acid and distributes heat generated by contraction; muscular pumps aid in venous return; exercise contributes to cardiovascular health.
Interplay of Systems Affecting Vitals
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Slide 10
NervousProduces cerebrospinal fluid (CSF); cardiac and vasomotor centers regulate cardiac output and blood flow through vessels via autonomic system
RespiratoryProvides blood for critical exchange of gases to carry oxygen needed for metabolic reactions and CO2 generated as byproducts of these processes
SkeletalProvides calcium, phosphate and minerals critical for bone matrix; transports hormones regulating buildup and absorption of matrix including erythropoietin stimulates myeloid cell hematopoiesis.
Urinary
Delivers 20% of resting circulation to kidneys for filtering, reabsorption and secretion of excess; regulates blood volume and pressure by regulating fluid loss in the form of urine and by releasing the enzyme renin, essential in the renin-angiotensin-aldosterone mechanism
Interplay of Systems Affecting Vitals
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Slide 11
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Slide 12
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Slide 13
Pulse Rate
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Slide 14 Pulse
• Stretch and recoil of the arterial wall during a cardiac cycle• Rate
• Number of beats per minute
• Rhythm• Interval between beats
• Volume – amount of blood pushed through the artery• Strength = ventricular contraction/cardiac output
• ↑ strength = ↑ systolic pressure• Bounding/full
• ↓ strength = ↓ systolic pressure• Weak/ thready
• Quality
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Slide 15 Variations in Pulse Wave• Pulsus alterans
• Alteration of weak and strong pulse beats not related to cycle length• Pericardial effusion
• Left ventricular failure
• Asthma
• Bigeminal pulse• Two beats close together with a pause following each pair
• Hypertrophic obstructive cadiomyopathy
• Hypothyroidism
• Electrolyte imbalance
• Paradoxical pulse• Exaggerated fall in systolic blood pressure with inspiration
• COPD
• Cardiac tamponade
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Slide 16 Pulse Assessment
Grade Pulse Description
0 Absent No perceptible pulse
1+ Thready Barely perceptible, easily obliterated with slight pressure
2+ Weak Difficult to palpate, slightly stronger than thready, can be obliterated with light pressure
3+ Normal Easy to palpate; requires moderate pressure to obliterate
4+ Bounding Very strong , hyperactive
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Slide 17 Factors Affecting Pulse
• Age• Infant = 100 - 130 bpm
• Child (1-7 yrs old) = 80 - 120 bpm
• Adult = 60 – 100 bpm
• Gender
• Emotional status
• Systemic or local heat
• Body size
• Exercise
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Slide 18 Effects of Aging
• Resting HR may be lower
• HR response is blunted• Rely more on Borg or BP response
• Heart Rate Reserve or Karvonen to determine target HR (closely approximates HR and VO2Max)• HRR=[((220-age)- Rest HR) X ____%] + Rest HR
• Beta Blockers
Borg RPE % of HRR % of 220-age
12-13 40-59% 55-69%
14-16 60-84% 70-89%
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Slide 19
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Slide 20
Blood Pressure
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Slide 21 Definitions
• Arterial Blood Pressure• Reflects the combined effects of arterial blood flow per minute
(cardiac output) and the resistance to that flow (peripheral vasculature)
• Systolic• Estimate of the work of the heart and the force of the blood against the
arterial walls during ventricular systole
• Diastolic• Heart’s relaxation phase
• Indicates peripheral resistance
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Slide 22 Classification of Hypertension (2017 Hypertension Guideline)
Classification Systolic blood Pressure (mm Hg)
Diastolic Blood Pressure (mm Hg)
Normal <120 <80
Prehypertension/Elevated
120-129 <80
Stage 1 hypertension
130-139 80-89
Stage 2 hypertension
> 140 >90
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Slide 23 Components of Arterial Blood Pressure (mm Hg)
Systolic/diastolic pressures• Hydrostatic Pressure
• Pressure exerted by blood on the walls of the heart or blood vessels
• Systemic arterial blood pressure = Cardiac Output X Total Peripheral resistance
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Slide 24 Components of Arterial Blood Pressure (mm Hg)
Pulse pressure• Difference between systolic and diastolic pressure
• Normal = 25% of systolic pressure • Below (called low or narrow)
• CHF (low stroke volume)
• Aortic valve stenosis
• Blood loss
• Above (high or wide) • Healthy individuals normal due to strenuous exercise (temporary)
• Chronically high = resistance in the arteries
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Slide 25 Components of Arterial Blood Pressure (mm Hg)
Mean arterial pressure• Average pressure of the blood in
the arteries• Normal range 70-110 mmHg• < 60 can result in ischemia and
hypoxemia
MAP=Diastolic BP + [0.333 (Systolic-Diastolic BP)]
Example: Patient with 127/89
102 mm Hg = 89 + [0.333(127-89)]
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Slide 26 Factors Affecting Arterial Blood Pressure
Cardiac Output• ↑ will cause an ↑ in BP
• Increased calcium ions, thyroid hormones, sympathetic stimulation, catecholamines
• ↓ will cause a ↓ in BP• Parasympathetic stimulation, elevated or decreased potassium ion levels,
decreased calcium levels, anoxia, acidosis
Compliance• Vascular disease causes “stiffening”
• Reducing compliance and increasing resistance to blood flow
• ↑ BP
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Slide 27 Factors Affecting Arterial Blood Pressure
Volume of blood• Hypovolemia (BP ↓)
• Bleeding, dehydration, vomiting, severe burns, antihypertensive medications
• Hypervolemia (BP ↑)• Retention of water and sodium
• CHF, liver cirrhosis, kidney disease, some steroid treatments
Viscosity of the blood• As viscosity ↑, resistance ↑ and flow ↓
• Anemia, polycythemia, cirrhosis, alcohol and drug toxicities, hepatitis
Blood vessel length and diameter• Obesity
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Slide 28 Physiological Variations in BP
Age• SBP and DBP gradually rise with age (after the age of 30)
• > in males
Circadian variation• Lowest during sleeps and highest in the mornings after waking up
Increases transiently during physical stress, anxiety, emotional excitement
When erect, BP in any vessel varies in relation to the vertical distance from heart level
• Orthostatic hypotension
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Slide 29 Regulatory Mechanisms for Blood Pressure
Vasomotor• Pons and upper medulla
• Produces a slow, continuous firing in all vasoconstrictor nerve fibers
• Normal vasomotor tone
Afferent Input• Baroreceptor
• Sensitive to stretch of vessel wall
• Concentrated at internal carotid arteries and above bifurcation of the aortic arch
• Chemoreceptor• Sensitive to decreased arterial oxygen concentration, increase in carbon dioxide, increase
in H+ ion concentration
• Carotid artery and aortic arch
• CN IX and X
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Slide 30
Homeostasis Restored
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Slide 31
Homeostasis Restored
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Slide 32
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Slide 33
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Slide 34
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Slide 35 Vital Signs: Blood Pressure
• Indirect method
• Cuff size matters• Too small, falsely high reading• Too large, falsely low reading
• Bladder width >40% of mid arm circumference
• Bladder length 80-100% of arm circumference
• Other sources of error• Arm position, rest period before,
body position, time between repeated measures, inflation/deflation method
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Slide 36 Automatic vs Manual Blood Pressure
• Determine if validated in patients with atrial fibrillation• Wide range of error in automatic
• 6.3 mmHg higher systolic BP in automatic
• Error with wrist cuffs• Positioning
• May lack sensitivity in patients with hypotension
• Finger devices not recommended
• Home blood pressure units have predictive value for morbidity and mortality
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Slide 37 Automatic vs Manual Blood Pressure
• Automated Blood Pressure Equipment is effective at detecting hypertension
• Is not reliable in detecting Hypotension
• Automated equipment has sensor looking for pulse pressure which is diminished when patient is hypotensive
• In presence of severe hypotension: can change to pediatric setting: less sensitive to pulse pressure
• Do you know how to adjust your equipment ???
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Slide 38 Recommended Technique(Chobanian, 2003; Whelton, 2017)
• Calibrate equipment
• Select appropriate cuff size
• Position cuff 1” above elbow crease and bladder centered over brachial artery
• Antecubital fossa at heart level resting comfortably with no muscle tension
• Patient should not talk or cross legs
• Increase pressure to 30 mm Hg above the level radial pulse extinguished
• Deflation rate at 2 mm Hg per beat
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Slide 39
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Slide 40 Recommended Technique (Chobanian 2003)
• Read the systolic level ( first sound of clear tapping, Phase I Kortkoff) and the diastolic level (the point at which the sound disappears, phase V Korotkoff)• If Korotkoff sounds persist to 0 mm Hg then use Phase IV
• Record BB to nearest 2 mm Hg on manometer and 1 mm Hg on electronic
• To avoid venous congestion should wait at least 1 minute between cuff readings
• Should be taken in both arms on the first visit to determine if one arm is consistently higher
• Document HR, BP, Position, arm used, Heart rhythm
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Slide 41
Respiratory Rate
Supply the body with oxygen for metabolic activity and to remove carbon dioxide
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Slide 42 Why should you take respiratory rate?
• Retrospective study: abnormal RR increased the odds of critical admission (OR = 1.66, 95% CI = 1.05-2.06) when compared to controls (Smith 2011)
• RR and HR are independent predictors of adverse events after discharge from ICU (Chaboyer 2008)• RR <10 or >25 (OR 4.23, 95% CI 2.12-8.45)
• Significant correlation (r = 0.84) between manual RR and continuous electronic monitoring (Smith 2011)
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Slide 43 The Respiratory System
• Inspiration• Contraction of the diaphragm and intercostal muscles
• Increases the intrathoracic space for lungs to expand
• Expiration• Passive during recoil of the lungs
• Pons and medulla serve as the respiratory cents• Control rate and depth of breathing in response to metabolic
needs
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Slide 44 Afferent Inputs• Chemoreceptors
• Central is in the respiratory center
• Sensitive to carbon dioxide and hydrogen ion levels
• Peripheral in the carotid bifurcation and arch of aorta• Sensitive to partial pressure of
oxygen
• Mechanoreceptors• Motor cortex
• Muscles and joint receptors
• Stretch receptors in the lung tissue and bronchioles
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Slide 45 Respiratory Assessment
Rate• Tachypnea >24 bpm
• Bradypnea < 10 bpm
Depth• Volume of air exchanged with each breath
Rhythm• Regularity of inspirations and expirations
Character• Deviation from normal quiet effortless breathing
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Slide 46 Patterns of Respiration
Type Description
Eupnea Normal respirations, with equal rate and depth, 12-20 breaths/min
Kussmaul’s Respirations Gasping, labored pattern
Biot’s Respirations Alternating periods of apnea and hyperapnea
Cheyne-StokesRespirations
Gradual increase in rate and depth, followed by gradual decrease
Apnea Absence of respiration
Paradoxical respirations Lung inflation during expiration, deflation during inspiration
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Slide 47 Factors Influencing Respiration
• Age• Newborns 30 - 50 bpm• Adults 12 – 18 bpm
• Body size
• Stature
• Exercise
• Body position
• Environment
• Emotion and Stress
• Drugs
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Slide 48 Peripheral Pulse Oximetry
Estimation of arterial oxyhemoglobin saturation (SaO2) by utilizing selected wavelengths of light to noninvasively determine the saturation of oxyhemoglobin (SpO2)
• Indirect measure
• Appropriate for continuous and prolonged monitoring• Smoking can provide a false increased reading
• Nail polish, dark skin or poor circulation can affect reading
The probe should be cleaned between patient applications according to manufacturer recommendations.
Documentation of results, therapeutic intervention (or lack of), and/or clinical decisions based on the SpO2 measurement should be noted in the medical record.
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Slide 49
Body Temperature
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Slide 50 Body Temperature
• Balance between the heat produced or acquired by the body and lost
• Maintain relatively constant internal body temperature
• Monitors to maintain optimal normal cellular and vital organ function
• Thermoreceptors• Provide input peripherally or centrally to the hypothalamus
• Regulating center• Coordination to maintain 37⁰C (98.6 + 1.8⁰ F)
• Effector organs• Include vascular, metabolic, skeletal muscle response
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Slide 51 Conservation of Body Heat
Vasoconstriction
• Hypothalamus activates sympathetic nervous system
• Vasoconstriction of cutaneous vessels
Decreased sweat gland activity
• To reduce or prevent heat loss by evaporation
• Sweating is stopped if body temperature falls below 37⁰C (98.6⁰F)
Cutis Anserina
• Hair standing on end (piloerection)
• Traps a layer of insulating air near the skin
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Slide 52 Production of Body Heat
Shivering
• Posterior hypothalamus
• Increased muscle tone
Hormonal Regulation
• Increase in norepinephrine and epinephrine
• Increase in thyroxin
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Slide 53 Increased Body Temperature
Pyrexia• Elevation of normal body temperature• Malaise, increased HR and RR, shivering, flushed skin
Hyperpyrexia• Extremely high temperature• Disorientation, confusion, seizure
Types• Intermittent• Remittent• Relapsing• Constant
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Slide 54
Hypothermia
• Lowered body temperature
• Decreased HR and RR. depression of mental and muscular responses, cyanosis, decreased cutaneous sensation
• Thermoregulatory center impaired at 34.4⁰C (94⁰F) and completely lost at 29.4⁰C (85⁰F)
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Slide 55 Factors Influencing Body Temperature
Time of Day
Age
Emotions
Exercise
External environment
Menstrual cycle
Pregnancy
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Slide 56 Healthy Exercise VitalsACSM 9th ed, Goodman and Snyder 4thed
• SBP Increases• In a linear fashion, 10 mm for every MET level
• 20 mm or more with min to mod exercise
• 40-50 mm with intense exercise
• SBP returns to pre-ex level in 5-7 min Pierson 2007
• HR rises linearly 10 BPM for each MET level
• HR returns to pre-ex level in 3-5 min
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Slide 57
Modify or Terminate
“Normals” with low number of Risk Factors
•SBP decreases 20•SBP >260•DBP >115•HR does not increase w/ ex•Angina, diaphoresis, pallor, nausea, confusion, ataxia, dizziness•Significant change in rhythm•RPE beyond target rangeACSM 9thed
Vitals Consideration with Exercise
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Slide 58
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Slide 59
Initiate when Do not initiate Modify or Terminate
Cardiac Pump Failure(EF defines degree of failure)Mild: 40-60%Moderate: 20-40%Severe: < 20%
Speaks without dyspneaWheezes < ½ lungsHR < 120Cahalin, 1996
‒ HR < 40, >130
‒ SBP > 180‒ DBP > 100‒ RR > 35O’Sullivan 4thed
‒ Dyspnea >3/10‒ RR >40‒ S3 Heart sounds appear‒ New/↑ wheezes‒ Pulse pressure < 10 ‒ HR or BP ↓ > 10-20‒ Increased Supraventricular and
ventricular ectopy‒ Angina, diaphoresis, pallor,
nausea, confusion, ataxia, dizziness
‒ SBP > 220‒ DBP > 115ACSM 9thed, O’Sullivan 4thed, Cahalin, 1996
Vitals Consideration with Exercise
Symptoms based approach! Collaboration with the healthcare team!
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Slide 60 Joint Commission as the 5th Vital Sign
• Information from the patient history• Pain characteristics
• Location and distribution
• Duration and periodicity
• Quality
• Associated signs and symptoms
• Management strategies
• Relevant medical history
• Relevant family history
• Psychosocial history
• Impact on daily life• Patient’s goals
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Slide 61 Joint Commission as the 5th Vital Sign
Unidimensional Pain Assessment Tools
• Numeric rating scale
• Visual analog scale
• Face pain scale
Multidimensional Pain Assessment Tools
• Brief Pain Inventory
• Initial Pain Assessment Inventory
• McGill Pain Questionnaire
• Memorial Pain Assessment Card
• Pain Drawing
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Slide 62 “Walking Speed: the Sixth Vital Sign”Fritz and Lusardi 2009
• 10 meter walk test • 5 m acceleration and 5 m deceleration
• Instructed to walk a comfortable pace
• Range for normal walking speed is 1.2-1.4 m/sec
• A change in .1 m/sec can be a predictor for improved health or a decline
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Slide 63 “Walking Speed: the Sixth Vital Sign”Fritz and Lusardi 2009
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Slide 64
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Slide 65 5 Meter Walk test
• Uses by STS (Society of Thoracic Surgeons) as predictor of Frailty
• Used with TAVR patient: pre and post op:
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Slide 66 Gait Speeds
• In acute care setting may be a better predictor of function and be considered as part of the discharge plan
• Gait speed rather that distance and FIM scores should be considered when determining safe discharge
• Should be utilized as part of the Physical Therapist Assessment in Acute Care
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Slide 67 Vital Signs are VITAL!
• Integrate into plan of care
• Look for trends
• Clinical decision-making
• Provides information on treatment presciption
• Accurate, documented vital signs are important
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Slide 68
Break
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Slide 69
Hemodynamic Monitoring and Invasive Lines
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Slide 70 Purpose
• Become more familiar with the hemodynamic monitoring devices
• Become more familiar with the numbers we see on the screen
• Plan– Explain 3 hemodynamic monitoring devices
• Arterial line
• Central venous line
• Swan line
– Explain the numbers seen on the monitor screen
– Determine safety to mobilize
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Slide 71 Safe?
“It is feasible and safe to provide progressive mobility activities in cardiovascular ICU patients with femoral catheters who meet the criteria for mobility interventions”
“provision of bedside physical therapy while patients underwent CRRT is feasible, and appears safe.”
“no significant contraindication to mobilize patients with femoral arterial/venous cannulation”
• Damluji, Abdulla, et al. "Safety and feasibility of femoral catheters during physical rehabilitation in the intensive care unit." Journal of critical care 28.4 (2013): 535-e9.
• Dubb, Rolf, et al. "Barriers and strategies for early mobilization of patients in intensive care units." Annals of the American Thoracic Society13.5 (2016): 724-730.
• Gokalp, Orhan, et al. "Cannulation in extracorporeal membrane oxygenation." Critical Care 18.4 (2014): 443.• Perme, Christiane, et al. "Safety and efficacy of mobility interventions in patients with femoral catheters in the ICU: a prospective
observational study." Cardiopulmonary physical therapy journal 24.2 (2013): 12.• Toonstra, Amy L., et al. "Feasibility and safety of physical therapy during continuous renal replacement therapy in the intensive care unit."
Annals of the American Thoracic Society 13.5 (2016): 699-704.• Wang, Yi Tian, et al. "Early mobilization on continuous renal replacement therapy is safe and may improve filter life." Critical Care 18.4
(2014): R161.
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Slide 72 Review A & P
• The heart
– anatomy
–Physiology• The plumbing
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Slide 73
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Slide 74
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Slide 75 Myocardial Conduction
• Sinoatrial Node (SA)– Pacemaker of the heart
– Cluster of cells ~ superior R atrium
• Atrioventricular Node (AV)– Slow conduction
• Bundle of His– Carry’s conductive signal from AV node to ventricles
• Purkinje Fibers– Carry signals into ventricles for contraction
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Slide 76
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Slide 77 Definitions of Heart Function
• Stoke Volume (L) ~70 ml– Volume of blood pumped by L ventricle in 1 beat
• Cardiac Output (L/min) ~ 5 L/m– Volume of blood pumped in 1 min
• Cardiac Index (CO/body weight)
• Ejection Fraction ****** Most important diagnostic measure of cardiac health
– % of volume ejected
– 60-67% Normal
– < 40% compromised cardiac dysfunction
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Slide 78
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Slide 79 Arterial line
• Where:
– Radial artery
– Femoral artery
– Brachial
– Axillary
– Dorsalis pedis
• Why?
– Arterial blood pressure (ABP)
– Oxygen saturation (SaO2)
– Source for serial blood gas draws• PaO2
• PaCO2
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Slide 80 Arterial Line
• Continuous arterial pressure monitoring
– Surgical procedures, CABG, other major surgeries or procedures
– All hemodynamic unstable patients
– Receiving potent vasopressor or vasodialator drugs
– IABP
– Need intracranial pressure monitoring
– Hypertensive crisis such as AAA, sepsis and stroke
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Slide 81 Arterial Line
• Serial blood gas measurements
– Respiratory failure
– Pt’s on or being weaned from mechanical support
– Acid/base abnormalities
– SaO2 more accurate reading than SpO2 saturation if peripherally compromised
Laboratory Values Interpretation Resource (updated January 2017)
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Slide 82 Mean Arterial Pressure
• MAP = [(2 x diastolic) + systolic] / 3 ...diastole counts twice as much because 2/3 of your cardiac cycle is in diastole
• A MAP of about 60mmHg is necessary to perfuse coronary arteries, brain, and kidneys.
• Arterial readings are higher than sphygmomanometer
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Slide 83 Considerations For Therapists
• Position of transducer to heart
– the transducer above the heart get a false low reading
– if below heart, have false high reading
• Enough slack
• Stopcock open to allow continuous flush
• Heparin bag needs to be pressurized
• If in femoral artery guarded activity in that leg (No ROM or flexion of hip)
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Slide 84 Arterial line
• Problems
– Ischemia or necrosis of the tissue
– Vascular insufficiency
– Infections
– Hemorrhagic disorders
– What are you going to do if you pull it out?
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Slide 85
110/70 mmHg
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Slide 86 Central Venous Pressure Line (CVP)
• Ie: Central line
• Where: tip located in superior and inferior vena cava
• How does it get there?– Subclavian
– R internal and external jugular
– Femoral
– Antecubital
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Slide 87
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Slide 88 CVP line Use
• Draw blood (serial draws)
• Provide fluids
• Invasive monitoring in the ICU/Critical Care or Surgery– Monitor central venous blood pressure
– Help determine right atrial (superior vena cava) pressure• Limited by respiratory variation and function
– Assess fluid volume status
– Administration potentially caustic medications
– Emergency route for pacemaker insertion
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Slide 89 Therapy Considerations
• Dysrhythmias with position changes
• Unstable patients may require supine position for accurate readings
• Maintain enough slack of lines
• Primarily a route for fluids, likely able to ambulate with CVP line
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Slide 90
6-12 mmHg
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Slide 91 Pulmonary Artery Catheter(Swan-Ganz)
• HJC Swan and Santa Monica Bay sailboats (NEJM 1970)
• Where: – Initiating @ external jugular
– Distal port in the pulmonary artery
– Proximal port in the right atrium
• How: place catheter into external jugular use balloon to float through heart and become wedged in pulmonary artery
Swan, H. J. C., et al. "Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter." New England Journal of Medicine 283.9 (1970): 447-451.
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Slide 92
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Slide 93 Swan Line
• What is it’s purpose?
– Distal port in pulmonary artery
• Pulmonary artery pressure (PA)
• Pulmonary artery wedge pressure (PAWP)• i.e. Pulmonary Artery Occlusion pressure (PAOP)
• Mixed venous draws (SVO2)
• Continuous flush
– Proximal Port
• Right atrial pressures (same as CVP)
• administer fluids
– Proximal injection for fluids
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Slide 94
–Thermistor for measurement:
• Stroke volume
•Central Venous Pressure (CVP)
•Cardiac output (CO)
•Cardiac index (CI)
–Measures by the temperature change and how long it take to get back to normal
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Slide 95 • Assesses circulatory volume (fluids) for many complex conditions:
– Heart failure– Shock– Burns– Renal disease– Many other cardiac dysfunctions
• Assessment of cardiovascular function for – complicated MI, severe CHF, structural defect
• Assessment of pulmonary status– cardiogenic vs. non-cardiogenic pulmonary edema, – acute respiratory failure– pulmonary hypertension
• Pre-op and post-op monitoring for complicated surgeries– (Cardiac, Organ Transplant, VAD placement)
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Slide 96 • Allows monitoring of all aspects of the heart
– Pulmonary artery
– Left and Right ventricle function
• Utilized for differential diagnosis– Pulmonary hypertension
– Cardiac tamponade
– Restrictive cardiomyopathy
• Pulmonary wedge/occlusion pressure• reflects left ventricular end diastolic pressure
• Assess left heart dysfunction
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Slide 97 Therapy Precautions
• Keep transducer at heart level
• Most accurate measurements are supine
• Each physician has differing comfort levels with mobilizing patients with Swan lines
• Maintain enough slack in line
• Watch for dysrhythmias
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Slide 98
http://bubbasoft.org/clinical-radiology
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Slide 99
12 vpm 5L 90-100%
35-45 mmHg
60 bpm
110/70 mmHg
15-25/6-12 mmHg
6-12 mmHg
HR should be similar
to confirm accuracy37oC
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Slide 100
Pulmonary Function Testing
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Slide 101
Tidal Volume (TV) The volume of air breathed in and out
without conscious effort
Inspiratory Reserve Volume (IRV) The additional volume of air that can be
inhaled with maximum effort after a
normal inspiration.
Expiratory Reserve Volume (ERV) The additional volume of air that can be
forcibly exhaled after normal exhalation.
Vital Capacity (VC) The total volume of air that can be
exhaled after a maximum inhalation:
VC=TV+IRV+ERV
Residual Volume (RV) The volume of air remaining in the lungs
after maximum exhalation. The lungs are
never completely emptied.
Total Lung Capacity (TLC) Vital Capacity+Residual Volume
Minute Ventilation The volume of air breathed in 1 minute
(TV) * breaths/minute
Pulmonary Function Testing
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Slide 102
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Slide 103 Pulmonary Function Testing
• Forced expiratory volume (FEV)
• Maximal airflow measured over 1 s (FEV1.0)
• Compare to predicted values (should be >80% of predicted)
• FEV1.0 /FVC ratio indicates pulmonary airflow capacity
• Reflects pulmonary expiratory power and overall resistance to air movement
• FEV1.0 /FVC = ~85% in healthy individuals
• FEV1.0 /FVC ≤70% = delineation point for airway obstruction (obstructive lung disease)
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Slide 104 Pulmonary Function Testing
How much air volume can be moved into and out of the lungs?
How fast the air in the lungs can be moved in and out?
How is the compliance of the lungs?
How do the lungs respond to chest physical therapy and medications?
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Slide 105 Pulmonary Function Testing
Uses
Screening for presence of obstructive or restrictive diseases.
Evaluating a patient prior to surgery.
Evaluate the patient’s condition for weaning from a ventilator.
Documenting the progression of pulmonary disease
Documenting the effectiveness of interventions
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Slide 106 Pulmonary Function Testing
Age- As a person ages the natural elasticity of the lungs
decreases which means smaller and smaller lung volumes as one
age.
Gender- Lung volumes for males are larger than those of
females even if they are matched for height and weight.
Body height and size- A small man will have a smaller
PFT result than a man of the same age who is much larger
Race- Environmental Factors and Altitude may have an affect
on PFT results.
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Slide 107 Pulmonary Function Testing
Terminology
• FVC- Forced Vital Capacity
• FEV1- Forced Expiratory Volume in 1 second
• FEV1/FVC- FEV1%- what percent of FVC is expelled in 1st second
• FEV3- Forced Expiratory Volume in 3 seconds
• FEV3/FVC- FEV3%- should be close to 100%
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Slide 108 Pulmonary Function Testing
FVC
• Obstructive lung disease- FVC will be decreased due to obstruction and airway collapse during forced exhalation.
• Restrictive lung disease FVC will be smaller due to the lungs being smaller to start with because of the disease.
• Bronchodilators will improve FVC 10-15% with obstructive lung disease.
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Slide 109 Pulmonary Function TestingSVC
Slow vital capacity (SVC) test- Have the patient
slowly and completely blow out all of the air from
their lungs. Eliminates the strong
bronchoconstriction that come with a forced
exhalation. The VC may be larger with a SVC test
leading to an obstructive diagnosis.
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Slide 110 Pulmonary Function TestingFEV1
• In healthy individuals it is common the exhale 75-80% of vital capacity in first second of FVC test.
• If FEV1 is low compared to predicted values the patient may have an obstructive or restrictive lung disease.
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Slide 111 Pulmonary Function TestingFEV1%
• Both FVC and FEV1 will be low in both obstructive and resistive lung disease.
• If FEV1% is low (<70%) it is consistent with an obstructive disease.
• If FEV1% is 85%-100% it is consistent with a restrictive disease.
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Slide 112 Examples of Pulmonary Function Tests in Normal Subjects and in Patients with Obstructive or Restrictive Lung Disease
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Slide 113 Pulmonary Function Testing
Lets Give It A Try
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Slide 114 Pulmonary Function Testing
Case 1
Predicted Values Measured Values % Predicted
FVC 6.00 liters 4.00 liters 67%
FEV1 5.00 liters 2.00 liters 40%
FEV1/FVC 83% 50% 60%
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Slide 115 Pulmonary Function Testing
Case 1
Predicted Values Measured Values % Predicted
FVC 6.00 liters 4.00 liters 67%
FEV1 5.00 liters 2.00 liters 40%
FEV1/FVC 83% 50% 60%
Obstructed Lung Disease
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Slide 116 Pulmonary Function Testing
Case 2
Predicted Values Measured Values % Predicted
FVC 5.68 liters 4.43 liters 78%
FEV1 4.90 liters 3.52 liters 72%
FEV1/FVC 84% 79% 94%
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Slide 117 Pulmonary Function Testing
Case 2
Predicted Values Measured Values % Predicted
FVC 5.68 liters 4.43 liters 78%
FEV1 4.90 liters 3.52 liters 72%
FEV1/FVC 84% 79% 94%
Restricted Lung Disease
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Slide 118 Pulmonary Function Testing
Case 3
Predicted Values Measured Values % Predicted
FVC 5.04 liters 5.98 liters 119%
FEV1 4.11 liters 4.58 liters 111%
FEV1/FVC 82% 77% 94%
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Slide 119 Pulmonary Function Testing
Case 3
Predicted Values Measured Values % Predicted
FVC 5.04 liters 5.98 liters 119%
FEV1 4.11 liters 4.58 liters 111%
FEV1/FVC 82% 77% 94%
Normal
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Slide 120 Obstructive Lung Disease
Emphysema- permanent enlargement of air-spaces distal to the terminal bronchiole with destruction of their walls.
Leading cause is SMOKING
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Slide 121 Emphysema
Clinical Presentation
Dyspnea- with exertion
Accessory muscle breathing
Pursed Lip breathing
Forward Posture
Barreled Chest
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Slide 122 EmphysemaClinical Presentation
Pink Puffers
Increased Respiratory Work
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Slide 123
Pink Puffer
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Slide 124 EmphysemaClinical Presentation
Reduced breath sounds in all lung fields
Wheezes
Increased Total Lung Capacity
Increased Residual Volumes
Increased dead Space
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Slide 125 Emphysema
Clinical Presentation
Chest X-ray
Over inflated Lungs
FlattenedDiaphragm
Elongated Heart
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Slide 126 Treatment
Non PT
Iv Fluids
Antibiotics
Low Flow O2
Bronchodilators
Corticosteriods
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Slide 127 TreatmentNote
Hypercapnia commonly occurs in severe Emphysema Oxygen
given to patients with emphysema may reduce their ability to
breath, resulting in hypercapnia. This is why exact doses of
oxygen are usually figured out for those with emphysema so that
they receive neither too little nor too much oxygen. Note: if a
patient is actively short of breath, never withhold oxygen from
them.
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Slide 128
Chronic Bronchitis
Chronic swelling and inflammation of the bronchi
and bronchioles
Diagnosis is based on a report of a productive
cough for 3 months during 2 consecutive years.
Obstructive Lung Disease
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Slide 129 Blue Bloater
Stocky
Appear blue
due to
hypoxemia
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Slide 130 Chronic Bronchitis
Blue Bloater
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Slide 131 Restrictive Lung DiseasePossible Causes
Pleural Effusion
Kyphoscoliosis
Obesity
Late Term Pregnancy
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Slide 132 Restrictive Lung Disease
Pulmonary Fibrosis
Sarcoidosis
Rheumatoid arthritis
Systemic Lupus Erythematosus
Scleroderma
Tuberculosis
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Slide 133 Restrictive Lung Disease
Decreased Vital Capacity
Decreased Inspiratory Capacity
Decreased Total Lung Capacity
Decreased lung compliance
Decreased diffusing capacity
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Slide 134
Lunch
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Slide 135
LIFE= VENTILATION + PERFUSION
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Slide 136 Now that we take the vital signs…….
• What next ?
• How do we use this information for clinical decision making
• How do we interpret vital signs ?
• How does this impact the plan of care ?
• What other factors do we need to consider that can affect vital signs?
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Slide 137 Other Factors Affecting Vital Signs
• Lab Values• Hgb
• Hct
• Sodium
• Potassium
• Calcium
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Slide 138 Other Factors Affecting Vital Signs
• Medications• Pressors
• Beta Blockers
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Slide 139 Other Factors Affecting Vital Signs
• CO2 Levels• Respiratory Acidosis• Respiratory Alkalosis
• Metabolic Causes• Metabolic Acidosis• Metabolic Alkalosis
• Vagal Responses
• Sepsis
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Slide 140
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Slide 141
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Slide 142
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Slide 143
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Slide 144 Vagal Episodes
• Vagal
• Holding their breath• Breathing is REQUIRED ! Not an
optional activity
• Valsalva• Decreased BP
• Decreased cardiac output
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Slide 145 Sepsis
• Accurate and timely assessment of vital signs can help with early diagnosis and treatment
• Vital signs and lab values are needed for complete assessment
• Putting all the pieces of the puzzle together
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Slide 146 Bringing Sepsy Back
• https://www.youtube.com/watch?v=58Y0OfOVzMo
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Slide 147 VITALS…. Are VITALLY Important
• Assessment of vital signs is a quality indicator
• EMR can be reviewed : random chart reviews
• Best Practice includes vital signs asessment
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Slide 148
How do we know we have proper perfusion?
The role of ICP, CPP, APP
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Slide 149
Cerebral Pressure and Perfusion
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Slide 150 Intracranial Components
• Brain parenchyma- 80%
• Cerebrospinal fluid (CSF) -10%
• Blood-10%
• Intracranial compartment is protected by the skull.
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Slide 151 CSF
• Clear liquid that surrounds the brain and spinal cord
• Essential for the protection and the brain
• Transporter of waste away from the brain and nutrients to the brain
• Brain’s 2nd circulation
• Produced in the ventricles
• We must have a balance of production and absorption for our brain to function normally
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Slide 152 Ventricles and CSF
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Slide 153 Ventricles and CSF
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Slide 154
Intracranial Pressure (ICP)
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Slide 155 Intracranial Components and ICP
• Volume is fixed in rigid skull
• An increase in any 1 of these components must be met with an equal decrease in another OR you have an increase in intracranial pressure (Monro-Kellie Doctrine)
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Slide 156 Intracranial Pressure (ICP)What is it?
• The pressure inside the skull and considered to be the result of the pressure in the brain tissue and the pressure that the cerebrospinal fluid (CSF) exerts in the ventricles and blood volume.• Total – Parenchyma (brain), blood and vessels, CSF)
• As intracranial blood volume goes up, so does the ICP
• Our body has a mechanism called autoregulation which can compensate for initial levels of increased ICP but has limited ability as these levels get higher.
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Slide 157 ICP
• Norms ~7–15 mmHg• Goal may be to keep it to >20 mmHg
• Intracranial Hypertension is diagnosed when ICP is at a sustained elevation ~37 mmHg
• Autoregulation can manage increased ICP up to 50 mmHg/day
• Increased intracranial pressure can lead to a medical emergency!
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Slide 158 Causes
• Due to a change in one of the components:
• CSF levels
• ↑ CSF production (meningitis, choroid plexus tumor, hemorrhage)
• Obstruction to CSF flow/absorption (Hydrocephalus)
• Volume of brain tissue
• Cerebral edema (brain injury, heart or liver failure)
• Edema volume added to the intracranial cavity
• Brain tumor, hematoma, abscesses)
• Changes in blood volume and flow
• Blood pooling or bleeding into part of brain
• Aneurysms, high blood pressure, stroke
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Slide 159 Signs and Symptoms
• Headache• Seizure• Nausea or Vomiting• Cranial nerve changes (blurred, double vision)• Changes in pupil appearance ((dilated, fixed, ipsilateral vs. bilateral)• Reflex changes• Changes in behavior• Problems with talking• Motor issues (weakness, paresis, posturing, hemiplegia)• Balance issues• Lack of energy or sleepiness
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Slide 160 Signs and Symptoms (continued)
• Posturing • Decerebrate: damage to midbrain and pons
• UE extension and external rotation; LE extension
• Decorticate: damage to the cerebral hemispheres • UE flexion (fist clenched) and internal rotation; LE extension
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Slide 161 Signs and Symptoms (continued)
• Incontinence
• Changes in level of consciousness
• Problems with command following
• Vital sign changes—increased temperature• Cushing’s triad
↑Blood Pressure
↓
Heart rate
Cushing’s Triad
↓
Respiratory Rate
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Slide 162
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Slide 163 ICP-How to Monitor
• External ventricular catheter or drain*• Gold standard
• Also known as a ventriculostomy
• Subarachnoid screw or bolt
• Intraparenchymal
• Epidural sensor
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Slide 164 External Ventricular Drain (EVD)
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Slide 165 External Ventricular Drains (EVD)
• What is it?• Catheter placed within the skull into the lateral ventricle which is connected
to a closed collecting device• A ventriculostomy is performed to create a hole within the ventricle for
drainage• If this drainage is temporary= EVD• If permanent drainage is in place= shunt
• Why is it used?• Allows drainage of CSF to relieve elevated intracranial pressure• Can be connected to a transducer that records ICP
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Slide 166 External Ventricular Drains
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Slide 167 External Ventricular Drains
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Slide 168 Treatment for Increased ICP
• Release of CSF through the external ventricular drain
• Positioning• Head of bed 30-45 degrees to increase cerebral venous drainage
• Environment (reduce stimuli)
• Blood pressure medication
• Sedation
• Osmotic diuretic (mannitol)
• Steroids
• Surgery (tumor excision, craniotomy)
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Slide 169
Cerebral Perfusion Pressure (CPP)
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Slide 170
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Slide 171 Cerebral Perfusion Pressure (CPP)- What is it?
• Blood flow to the brain!!• Pressure at which the brain is perfused
• About 15-20% of cardiac output
• Best indicator of brain perfusion
• Lack of blood flow= impaired oxygen and metabolic delivery and ultimately loss of brain tissue
• Impacted by mean arterial pressure and intracranial pressure
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Slide 172 Cerebral Perfusion Pressure (CPP)
•CPP= mean arterial pressure [MAP]- ICP
• CPP goals are 60-70 mmHg or ≥ 60 mmHg• 50 mmHg is critical level for occurrence of brain ischemia
• SAMPLE CALCULATION:• MAP of between 60 to 80 mmHg and an ICP about 10 mmHg
• CPP= (60-80) minus 10
= 50-70 mmHg
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Slide 173 Decreased Cerebral Perfusion Pressure
•How does the body react to
changes in CPP?
Body senses decreased CPP and ischemia
Senses decreased systemic blood
pressure
Dilates cerebral blood vessels
Increased cerebral blood
volume
This increases ICP
This leads to decreased CPP
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Slide 174 CPP- Implications
• Higher ICP from injury will require a higher CPP to maintain cerebral blood flow • Decreases in ICP can also positively impact cerebral perfusion HOWEVER in
most cases the MAP is adjusted to control CPP
• Blood pressure could be kept HIGHER to ensure adequate cerebral perfusion.
• Patients administered vasopressor agents to increase MAP• may lower ICP by improving perfusion
• allowing autoregulatory vasoconstriction as ischemia is relieved and ultimately decreasing intracranial blood volume
• Mortality increases approximately 20% for each 10 mmHg loss of CPP
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Slide 175 Considerations for Rehab Professionals
• Patients may be sedated to try and reduce ICP• Reduction of metabolic demand
• Be aware of ICU’s parameters for the ICP before starting PT • If patient has an ICP of ~20, you may want to hold PT due to impact of elevation of
ICP on CPP
• Report changes in ICP during session• Changes that last ≥ 5 minutes are more concerning than brief changes
• Be aware of the ICP value and waveform on the monitor. The waveform may change shape if cerebral hypoxia or ischemia occurs.
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Slide 176 Considerations (continued)
• EVDs must be clamped • before getting out of bed, changing body position
from supine, or adjusting angle of bed
• Keep slack in the lines
• Must bring EVD collection bag/lines with mobility—2nd set of hands needed
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Slide 177 Considerations (continued)
• Patients with elevated ICP are positioned with head of bed (HOB) elevated at 30◦ to maximize venous flow. • Lowering HOB may increase ICP.
• Lateral neck flexion and extreme hip flexion may increase ICP
• Changing patient position in bed (sliding down) could affect drainage system
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Slide 178 Considerations (continued)
• Patient may only tolerate short bouts of activity.
• Monitor for signs and symptoms of ICP changes • headache, confusion, dizziness
• Monitor Glasgow Coma Scale score changes especially if patient has a brain injury
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Slide 179 Considerations (continued)
• ICP Normal: ~7-15 mm Hg
• ICP >20 mmHg (GCS 13-15)• patient drowsy and confused
• ICP > 30 mm Hg (GCS <8) • severe brain swelling
• patient non-participatory
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Slide 180
Abdominal pressure and perfusion
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Slide 181 Abdomen and Abdominal Cavity
• Organs
• Blood vessels
• Peritoneum
• Muscles
• Fascia
• Skin
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Slide 182 Intra-abdominal Pressure (IAP)
• Our abdomen has a steady state pressure in our abdominal cavity.
• Pressure changes occur:• With postural changes• With movement of diaphragm• Physical activity• Coughing• Straining• Organ dysfunction• Fluid overload• Pregnancy
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Slide 183 Intra-abdominal Hypertension(IAH)
• When IAP is sustained ≥12 mm Hg the patient now has intra-abdominal hypertension
Types of Intra-abdominal Hypertension (IAH)
Definition Cause
Hyperacute Elevation of IAP lasting for seconds
From coughing, sneezing, straining, physical activity
Acute Elevation of IAP that lasts for hours
Result of trauma or intra-abdominal hemorrhage
Subacute Elevation of IAP that lasts for days
Common with medical patientsand can last for days
Chronic Elevation of IAP that develops over months or years
Pregnancy or morbid obesity
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Slide 184 Intra-abdominal Hypertension-Systemic Effects
Central Nervous System
Pulmonary
Cardiovascular
Kidney
Gastrointestinal
System Effects
Central Nervous System Cardiac System Pulmonary System
↑ Intracranial pressure Hypovolemia ↑ Intrathoracic pressure
↓ Cerebral perfusion pressure ↓ Cardiac output ↑ Airway pressure
Renal Function ↓ Venous return ↑ Peak inspiratory pressure
↓ Urinary output ↑ SVR ↓ Compliance
↓ Renal blood flow and ↓ GFR ↑PCWP and CVP ↑ Ventilation/perfusion Mismatch
Hepatic Function GI Function ↓ Functional residual capacity
↓ Portal blood flow ↓ Mucosal, celiac and SMA blood flow
↑ PaCo2
↓ Lactate clearance ↓ Renal blood flow ↓ PaO2
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Slide 185 Symptoms
• Tensely distended abdomen—classic sign
• Patients are critically ill and may be unable to communicate• Complaints of weakness, shortness of breath, abdominal pain, abdominal
bloating.
• As levels get higher they may need ventilator support.
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Slide 186 Transition of IAP to Abdominal Compartment Syndrome
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Slide 187 Abdominal Compartment Syndrome (ACS)
• What is it?• Organ dysfunction that is caused by intra-abdominal hypertension
• Etiology• Injury or disease in the abdominopelvic region (pancreatitis, abdominal trauma)
• Severe burns
• Liver transplantation
• Trauma patients in shock with aggressive fluid resuscitation
• Medicine patients needing fluid resuscitation
• Post-surgical patients who are given large volume resuscitation
• Retroperitoneal conditions (ruptured AAA, pelvic fracture with bleeding, pancreatitis)
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Slide 188 Treatment of ACS and IAH
• Supportive care• reduce intra-abdominal volume through avoidance of adding extra fluid
• evacuation of intra-abdominal space-occupying lesions (i.e. ascites, hematoma)
• evacuation of intraluminal bowel contents
• improve abdominal wall compliance (pain meds and sedation)
• nasogastric and rectal drainage for patients with bowel distension
• positioning in supine to avoid increases in IAP
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Slide 189 Treatment (continued)
• Surgical care• Open abdominal decompression with temporary abdominal closure
• May have temporary closure for days/weeks
• Could have open abdomen with closed or open fascia
• May be on a suction device
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Slide 190 How to monitor intra-abdominal pressure
• Bladder catheter*
• Inferior vena catheters
• Intragastric catheters
• Intracolonic catheters
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Slide 191
Abdominal Perfusion Pressure (APP)
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Slide 192 Abdominal Perfusion Pressure (APP)- What is it?
• Blood flow to the abdominal viscera!!
• High IAP leads to a lack of blood flow= impaired oxygen and metabolic delivery and ultimately loss of tissue, organ failure, and death
• Impacted by mean arterial pressure and intra-abdominal pressure
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Slide 193 Abdominal Perfusion Pressure (APP)
•APP= mean arterial pressure [MAP]- IAP
• APP norms are 60-70 mmHg
• A target APP of at least 60 mmHg is correlated with improved survival from IAH and ACS
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Slide 194 Considerations for Rehab Professionals
• Be aware of the APP and IAP levels before seeing patient and monitor during the session
• Be aware of what was done for open abdominal closure procedure• Open abdomen with open fascia- will be the most restrictive (may allow ROM
only)
• Open abdomen with closed fascia- may allow mobility with binder in place
• Be aware that changes in bed position will impact IAP• Some patients will need to be on bed rest
• These patients may be on sedation
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Slide 195 Considerations (continued)
• Patients who are s/p open abdominal decompression are STILL at rest for elevated IAP and for development of IAH and ACS
• Watch for signs of ischemia• Claudication pain
• UMN signs in the lower extremities (spinal cord ischemia)• weakness (no muscle wasting)
• clonus
• ↑ tone (may start out flaccid but then changes)
• ↑ reflexes
• + Babinski
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Slide 196
Break
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Slide 197
EKGElectrocardiography
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Slide 198
Cardiac Action Potential
• Phase 0- depolarization- Na+ channels open
• Phase 1-prolonged action potential due to slow and extended opening of Ca+ channels -repolarization begins.
• Phase 2-outward flow of K+ and prolonged opening of Ca lead to a plateau phase
• Phase 3- closure of Ca channels and opening of K channels completes repolarization.
• Phase 4- resting phase Na and Ca are pumper out K is pumped in.
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Slide 199
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Slide 200
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Slide 201
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Slide 202
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Slide 203
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Slide 204
EKG
• 12 Lead (view) of the heart
• Six Leads record frontal plane
• Six Leads record transverse plane
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Slide 205
Frontal Plane Leads
• 3 Bipolar limb leads I, II, III
– Single positive and single negative electrode
• 3 augmented unipolar limb leads
– aVR (right arm)
– aVL (left arm)
– aVF (left leg)
Have single positive lead derive negative from a combination of other electrodes.
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Slide 206
Einthoven’s Triangle
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Slide 207
Bipolar Leads
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Slide 208
Augmented Leads
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Slide 209
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Slide 210 Axis Deviation
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Slide 211 Axis Deviation
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Slide 212
Precordial (transverse plane) Leads
• V 1-6
• V1 and V2 look at R Ventricle
• V3 and V4 look at the intraventricular septum
• V5 and V6 look at L Ventricle
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Slide 213
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Slide 214
EKG Evaluation
• What is the rate and pattern (regularity) is R-R interval equal for each beat?
• Is the a P wave before each QRS? = atrial
• Is the a QRS after every P wave?= conduction of atria to the ventricles
• P-R interval? Normal= 0.12-0.2 seconds > 0.2 seconds= conduction delay or block
• QRS normal duration (0.1 sec) and shape?
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Slide 215
Calculating Rate
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Slide 216
Calculating Rate
• Count the number of small boxes between two R waves and divide into 1500.
• Count the number of R waves in a six second strip and multiply by 10.
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Slide 217 Lets try it
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Slide 218
Sinus Rhythms
• Sinus Rhythm- 60-100 bpm
• Sinus Bradycardia- < 60 bpm
• Sinus Tachycardia- > 100 bpm
• These rhythms have normal P waves, PR int and QRS int
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Slide 219
Supraventricular Dysrhythmias
Atrial and Junctional Mechanisms
– Supraventricular tachycardia (SVT)
–Atrial tachycardia
–Atrial Flutter
–Atrial Fibrillation
– Junctional Rhythm
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Slide 220 SVT
Rate- 150-250- regular rhythm- no visible P waves- PR not measurable-QRS .12 or less
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Slide 221 Atrial Tachycardia
Rate 150-250- regular- 1 P per QRS- PR may be shorter, QRS .12 or less
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Slide 222 Atrial Flutter
Atrial rate 250-450- ventricular varies- Atrial is regular-ventricular can be irregular- P wave- saw tooth- PR not
measurable- QRS <.12.
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Slide 223
Atrial FibrillationRate can vary- Irregularly Irregular- P waves chaotic- PR not measured- QRS <.12.
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Slide 224 Junctional RhythmRate- 40-60- regular- P waves inverted-before or after QRS or absent- PR if
present <.12- QRS .12 or less.
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Slide 225 Ventricular Dysrhythmias
Premature Ventricular Contraction (PVC)
–Bigeminy
–Ventricular couplet
–Multifocal PVC (>1 ectopic focus)
Ventricular Tachycardia
Ventricular Fibrillation
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Slide 226 PVC
Rate varies- Can be regular or irregular- P wave will be absent-unmeasurable PRI- QRS >.12.
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Slide 227 Bigeminy
1 PVC every other beat- regular-irregular rhythm
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Slide 228 Ventricular Couplet
PVC occurs twice
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Slide 229 Multi-Focal PVC
Can be both positive and negative since there are different ectopic origins
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Slide 230 Ventricular Tachycardia
3 or more PVC with rate >100 bpm- patient can be asymptomatic-symptomatic or unconscious and pulseless.
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Slide 231 Ventricular Fibrillation
No organized rhythm- needs immediate defibrillation
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Slide 232
Atrioventricular Blocks
First Degree AV Block
Second Degree AV Block• Mobitz Type 1- Wenckebach
• Mobitz Type 2
Third Degree AV Block
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Slide 233 First Degree Heart Block
PR interval > .20s
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Slide 234 Mobitz Type 1
PR interval progressively get longer than QRS drops
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Slide 235 Mobitz Type 2
Regular dropped QRS every 2nd third or 4th P wave- consistent PR interval
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Slide 236 Third Degree Heart Block
No conduction between A and V- both will have regular rates- Ps can be hidden in QRS
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Slide 237 Story of the AV block Family
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Slide 238 Bundle Branch Blocks
• Right Bundle Branch Block RBBB
• Left Bundle Branch Block LBBB
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Slide 239 Left Bundle Branch Block
• Increased QRS >.10s
• Once a widened QRS > 0.10s is identified, we look at leads closest to the LV to identify a LBBB.Leads V5,V6, I, and aVL are in close proximity to the left ventricle, and as such, are the best location to identify a LBBB.
• Characterized by an RSR segment or notched QRS
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Slide 240
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Slide 241 Right Bundle Branch Block
Look at Right chest Leads V1 and V2
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Slide 242
Myocardial Infarction
• ST segment elevation
• ST segment depression
• Inverted T wave
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Slide 243
ST segment elevation
• Transmural MI
• Use precordial leads to localize
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Slide 244
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Slide 245
ST segment depression
• Myocardial ischemia- can be diagnostic during exercise
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Slide 246
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Slide 247
Inverted T wave
• Myocardial ischemia (can be old)
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Slide 248
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Slide 249
EKG Lab
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Slide 250 Case 1
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Slide 251 Case 2
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Slide 252 Case 3
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Slide 253 Case 4
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Slide 254 Case 5
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Slide 255 Case Studies
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Slide 256
Game Show Wrap Up
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Slide 257 References Academy of Acute Care Physical Therapy (2017). Laboratory Values Interpretation Resource. Retrieved from
http://www.acutept.org/?page=ResourceGuides American Physical Therapy Association. (2016). Guide to Physical Therapy Practice 3.0. Alexandria: American Physical
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Therapy Association. Retrieved from www.apta.org: http://guidetoptpractice.apta.org/site/misc/terms.xhtml American Physical Therapy Association. (2016, May). The Movement System Brings it All. PT in Motion, 8(4), 14-21. American Physical Therapy Association, Movement System. http://www.apta.org/MovementSystem/. Accessed
10/30/2017. Anatomy and Physiology: Homeostatic regulation of the Vascular System. http://philschatz.com/anatomy-
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Phys Ther. 27, 57. Burlew Cn et al. Trauma. In: Brunicardi F, et al. (ed). Schwartz's Principles of Surgery, 10e New York, NY: McGraw-Hill;
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Slide 258 References Cahalin, L.P., Mathier, M.A., Semigran, M.J., Dec, G.W., Disalvo, T. G. (1996). the six-minute walk test predicts peak
oxygen uptake and survival in patients with advanced heart failure. Chest, 110(2), 325-32. Chaboyer, W., Thalib, L., Foster, M., Ball, C., Richards, B. (2008). Predictors of adverse events in patients after
discharge from the intensive care unit. Am J Crit Care, 17(3), 255-63. Daamen, M. A. M. J., Brunner-la Rocca, H. P., Tan, F. E. S., Hamers, J. P. H., & Schols, J. M. G. A. (2017). Clinical
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Damluji, Abdulla, et al. "Safety and feasibility of femoral catheters during physical rehabilitation in the intensive care unit." Journal of critical care 28.4 (2013): 535-e9.
Dubb, Rolf, et al. "Barriers and strategies for early mobilization of patients in intensive care units." Annals of the American Thoracic Society 13.5 (2016): 724-730.
Fields, C., Trotsky, A., Fernandez, N., & Smith, B. A. (2015). Mobility and Ambulation for Patients With Pulmonary Artery Catheters: A Retrospective Descriptive Study. Journal of Acute Care Physical Therapy, 6(2), 64-70. doi:10.1097/JAT.0000000000000012
Fritz, S., Lusardi, M. (2009). White: paper: “Walking speed: the sixth vital sign.” J Geriatr Phys Ther, 32(2), 46-9. Frownfelter, D., & Dean, E. (2012). Cardiovascular and Pulmonary Physical Therapy Evidence and Practice (5th ed.).
St Louis: Elsevier-Mosby. Gestring, M. Abdominal Compartment Syndrome in Adults. In: UpToDate, Sanfey H (Ed), UptoDate, Waltham, MA,
2017. Goodman, C. C., & Fuller, K. S. (2015). Pathology Implications for the physical therapist. St Louis: Elsevier Saunders. Gokalp, Orhan, et al. "Cannulation in extracorporeal membrane oxygenation." Critical Care 18.4 (2014): 443.
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Slide 259 References Haines KJ, et al. Association of postoperative pulmonary complications with delayed mobilization following major
abdominal surgery: an observational cohort study. Physiotherapy 99 (2013) 119-125. Hall, J. B., Schmidt, G. A., & Kress, J. P. (2015). Principles of Critical Care. New York: Mcgraw-Hill Education. Hedges JS. et al. Chapter 4 Early Rehabilitation Interventions. In: Robinson LR (ed). Trauma Rehabilitation: Wolters
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Waltham, MA, 2017.Hemphill JC et al. Neurologic Critical Care, Including Hypoxic-Ischemic Encephalopathy, and Subarachnoid Hemorrhage In: Kasper D et al.(ed). Harrison's Principles of Internal Medicine, 19e. New York, NY: McGraw-Hill Education; 2014.
Ho VP, Barie PS. Acute Abdominal Dysfunction. In: Oropello JM, et al.. eds. Critical Care New York, NY: McGraw-Hill; Joyner, M. J., Casey, Darren, D. P. (2015). Regulation of Increased Blood Flow (Hyoeremia) to Muscles During Exercise:
A Hierarchy of Competing Physiological Needs. Physiol Rev, 95(2): 549-601. Kasper DL, et al. eds. Increased Intracranial Pressure and Head Trauma. In: Harrison's Manual of Medicine, 19e New
York, NY: McGraw-Hill; Kerr M, Crago EA. Nursing management: acute intracranial problems. In: O'Brien PG, Giddens JF, Bucher L, eds.
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Slide 260 References Lyell, D., & Coiera, E. (2016). Automation bias and verification complexity: a systematic review. Journal of the American
Medical Informatics Association, 24(2), 423-431. Malone, D., Ridgeway, K., Norton-Craft, A., Moss, P., Schenkman, M., & Moss, M. (2015). Physical therapist practice in
the Intensive care Unit: results of a National Survey. Physical therapy, 95, 1335-1344. doi:10.2522/ptj.20140417 Malone DJ, Lindsay KLB. Physical therapy in acute care : a clinician's guide. Thorofare, NJ: Slack; 2006. Mariano GL, et al. Intracranial Pressure: Monitoring and Management. In: Hall JB, eds. Principles of Critical Care, 4e
New York, NY: McGraw-Hill; 2014. Martin, N. Management of the open abdomen in adult. In: UpToDate, Bulger EM (Ed), UpToDate, Waltham, MA, 2017. Matuskowitz, A. J., Carr, C. M., Jennings, L., Hall, G. A., & Saef, S. H. (2016). 107 How Good are Paramedics and
Emergency Physicians at Diagnosing a STEMI by EKG Compared to Cardiologists?. Annals of Emergency Medicine, 68(4), S43.
Mufti, T. S., Durkhanay W. (2016). Accuracy of Blood Pressure recording by Manual and Automated Digital Devices: A Clinical Guideline. J Rehman Med Inst, 2(2), 17-25.
Oropello JM, Mistry N, Ullman JS. Head Injury. In: Hall JB, Schmidt GA, Kress JP. eds. Principles of Critical Care, 4e New York, NY: McGraw-Hill; 2014.
O’Sullivan, S., Schmitz, T., Fulk, G. (2014). Physical Rehabilitation. 6th ed. Parry, S. M., Granger, C. L., Berney, S., Jones, J., Beach, L., El-Ansary, D., . . . Denehy, L. (2015, Feb 5). Assessment of
impairment and activity limitations in the critically ill: a systematic review of measurement instruments and their clinimetric properties. doi:10.1007/s00134-015-3672-x
Paz J. Michelle West. Acute Care Handbook for Physical Therapist 4th edition St. Louis, Mo: Elsevier; 2014.
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Slide 261 References Paz J, West M. Acute care Handbook for Physical Therapists. 3rd ed. St. Louis: Saunders Elsevier; 2009 Perme, Christiane, et al. "Safety and efficacy of mobility interventions in patients with femoral catheters in the ICU: a
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Slide 262 References
Smith, I., Mackay, J., Fahrid, N., Krucheck, D. (2011). Respiratory rate measurement: a comparison of methods. British Journal of Healthcare Assistants. 5(1), 18-23.
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