defining the undefined in critical rehabilitation · defining the undefined in critical care...

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Defining the UndefinedIn Critical Care RehabilitationErica Colc lough PT, CCS

Ti ffany Haney PT, CCS

Stephen Ramsey PT, DPT, CCS

Disclosures

• We have no relevant financial relationships to disclose

Learning Objectives

1. Discuss effects of vasoactive medications, mechanical ventilation and mechanical circulatory support on cardiac output.

2. Discuss methods to improve early mobility of patients who are being mechanically ventilated, including order set options, and alternative weaning strategies/protocols

3. Understand advanced mechanical and circulatory methods of assisting the cardiac and pulmonary systems, and be able to determine appropriate mobility programs for patient

4. Discuss evidence for mobility of patients requiring advanced circulatory and mechanical assist devices as well as indications/contraindications for mobility

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Course Outline

I. Case presentation

II. Medical management of Heart FailureI. CompensatedI. Medications

II. Hemodynamics

II. Decompensated

Course Outline

III. Supplemental Oxygen

I. NIPPV

II. IPPV

• Early mobility

• Parameters

• SBT/SAT

• Interventions to assist with weaning

Course Outline (Cont.)

IV. Intra‐aortic Balloon Pump (IABP)I. Indications

II. Current Evidence for mobility

III. Mobility with femoral insertion

IV. Hemodynamic monitoring

V. Extra‐corporeal Membrane Oxygenation (ECMO)I. Veno‐Arterial vs. Veno‐Venous

II. Variation in cannulation

III. Mobility criteria

IV. Current evidence

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Course Outline (Cont.)

VI. Advanced Surgical OptionsVI. Left Ventricular Assist Device (LVAD)

VI. Indications

VII. Pre‐LVAD frailty screen

VIII. Current evidence

Poll Questions

Respond at: https://pollev.com/ellenhillega921

Respond at: https://pollev.com/ellenhillega921

1

Text Ellenhillega921to 37607, then respond A, B, C, D

Text Ellenhillega921to 37607, then respond A, B, C, D

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Case Presentation

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Past Medical History (PMHx)

oMr. Shock is a 44 year old male with PMHx significant for:o Sleep apnea (02/2017)o Nonischemic cardiomyopathy (NICMO)o Chronic systolic CHF (congestive heart failure)o Atrial flutter s/p CTI ablation (01/2008) on Pradaxao Dual chamber pacemaker/defibrillator (10/2004)o Chronic kidney diseaseo Diabetes mellitus type 2o Dyslipidemia o Gastroesophageal reflux disease (GERD)o Peripheral artery disease.

oMobility limited by DOE. Ambulates short distances without DME.

History of Present Illness (HPI)

oHe presented to the outpatient heart failure clinic on 10/16/17 with heart failure exacerbation, complaining of dyspnea on exertion, orthopnea, loss of appetite, and weight gain of 20 lbs. despite adherence to diuretics.

oHe was admitted directly from the heart failure clinic to the cardiac telemetry floor on 10/16 for close monitoring and medical optimization.

Pertinent Imaging

oECHO on 10/17 revealed severe LV dilation, LA dilation, moderate mitral regurgitation. Ejection fraction of 30%. Severe RV dilation with reduced RV systolic function. PA pressures moderately elevated, with mean of 28 mmHg. Moderate tricuspid regurgitation and moderately dilated RA.

oCXR on 10/17 showed bilateral pulmonary infiltrates consistent with pulmonary edema. Mild blunting of costophrenic angles, evidence of mild pleural effusion. Cardiomegaly.

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Heart Failure

1

Left Ventricular DysfunctionHigh Pressures

Hypertrophy

Diastolic Dysfunction

Preserved EF

Large Volumes

Dilation

Systolic Dysfunction

Reduced EF

Treating Heart Failure

Primary Goal of Drug Therapy in Heart Failure:

Increase stroke volume

Reduce clinical symptoms

Primary Goal of Drug Therapy in Heart Failure:

Increase stroke volume

Reduce clinical symptoms

Systolic Dysfunction:

Guideline‐Directed Medical Therapy

Systolic Dysfunction:


Diastolic Dysfunction:

No consensus

Diastolic Dysfunction:

No consensus

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Stroke Volume FormulaSV = LVEDV ‐ LVESV

Stroke Volume3 Factors1. Preload

AKA: LV Filling/LVEDP

2

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Stroke Volume3 Factors

1. Preload

2. Afterload

AKA: Resistance/SVR

3

Stroke Volume3 Factors

1. Preload

2. Afterload

3. Contractility

AKA Inotropy/Squeeze

4

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Treating Heart Failure

•Increase contractility

•Decreasing HR

Increase Forward Flow by:

•Decreasing afterload

•Reach euvolemia

Decreasing Backup of Flow by:

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Physical Examo A thorough history and physical examination should be obtained/performed in patients presenting with HF to identify cardiac and noncardiac disorders or behaviors that might cause or accelerate the development or progression of HF (LOE C. Class I) 5

o Volume status and vital signs should be assessed at each patient encounter. This includes serial assessment of weight, as well as estimates of jugular venous pressure and the presence of peripheral edema or orthopnea (LOE B. Class I) 5

Physical Examo A thorough history and physical examination should be obtained/performed in patients presenting with HF to identify cardiac and noncardiac disorders or behaviors that might cause or accelerate the development or progression of HF (LOE C. Class I)

o Volume status and vital signs should be assessed at each patient encounter. This includes serial assessment of weight, as well as estimates of jugular venous pressure and the presence of peripheral edema or orthopnea (LOE B. Class I)

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Physical Exam

COMPENSATED HEART FAILURE

o Vitals: Adequate BP and HR

o Lungs: Clear

o Heart: +/‐ S3/S4. No JVD

o Extremities: Warm and non‐edematous

o Neuro: Intact

o Kidneys: Adequate UOP

MR. SHOCK 10/17

o Vitals: 118/62 mmHg. HR 82 bpm

o Lungs: Slight rales in bases only

o Heart: + S3. No JVD.

oExtremities: Warm. 1+ edema BLE

o Neuro: A&O x4

o Kidneys: Increase UOP with IV duiretics

Evidence of Congestion

No Yes

NoWarmDry

WarmWet

YesCold Dry

Cold Wet

Evidence of Low Output


No Yes

NoWarmDry

WarmWet

YesCold Dry

Cold Wet

Evidence of Low Output

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o Ace inhibitor/ARB

o Beta Blocker

o Aldosterone Antagonists

o Hydralazine/Nitrates

o Diuretics (If needed)

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o Ace inhibitor/ARB

o Beta Blocker




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o Ace Inhibitors o RAAS suppressiono Dilate arteries and veins by blocking

angiotensin II formation and inhibiting bradykinin metabolism.

o ARBso Dilate arteries and veins by

preventing angiotensin II bindingo For ace inhibitor intolerance

(cough/angioedema)o PT Application

o Hypotension with mobilityo Cough and angioedema with ACE

DECREASE AFTERLOADDECREASE PRELOAD

Evidence5

o The clinical strategy of inhibition of RAAS with ACE inhibitors in conjunction with evidence‐based beta blockers, and aldosterone antagonists in selected patients, is recommended for patients with chronic HFrEF to reduce morbidity and mortality. (LOE A. Class I )

o The use of ARBs to reduce morbidity and mortality is recommended in patients with prior or current symptoms of chronic HFrEFwho are intolerant to ACE inhibitors because of cough or angioedema. (LOE A. Class I)

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o Ace inhibitor/ARB

o Beta Blocker




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o Beta‐Blockero Competitive binding to beta

adrenoceptors.o SNS inhibition, decreases HR.o Slows HF progression, reduced

hospitalizationo PT Application

o Blunted HR rise with activityo Use RPE/dyspnea scale for symptom

limited exercise

DECREASE INOTROPYINCREASE PRELOAD

Evidence 5

o In all patients with a recent or remote history of MI or ACS and reduced EF, evidence‐based beta blockers should be used to reduce mortality. (LOE B. Class I)

o Beta blockers should be used in all patients with a reduced EF to prevent symptomatic HF, even if they do not have a history of MI. (LOE C. Class I)

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o Ace inhibitor/ARB

o Beta Blocker




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Guideline‐Directed Medical TherapyoAldosterone Antagonist

oDiuresis by inhibiting Na+ reabsorptiono K+ sparing

oPT ApplicationoHypotensionoDehydration

DECREASE PRELOADDECREASE AFTERLOAD

Evidence 5

o Aldosterone receptor antagonists are recommended to reduce morbidity and mortality following an acute MI with EF of 40% or less, who develop symptoms of HF or have a h/o DM. (LOE A. Class I. )


o Ace inhibitor/ARB

o Beta Blocker




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o Hydralazine/Nitrateso Hydralazine (Arteries)o Nitrates (Veins)o Should be used in all patients

unable to take ACE/ARB or those hypertensive on ACE/ARB

o PT Applicationo Hypotension with mobility

DECREASE PRELOADDECREASE AFTERLOAD

Evidence 5

oThe combination of hydralazine and isosorbide dinitrate is recommended to reduce M/M in patients with NYHA class III‐IV, HFrEF, receiving therapy with ACEi and BB, unless contraindicated (LOE A. Class I)

o For persistently symptomatic patients, NYHA III‐IV, Stage C or D, add hydralazine and nitrates (LOE A. Class I).

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o Ace inhibitor/ARB

o Beta Blocker




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o Loop Diureticso Thiazide Diuretics

o Inhibit Na, Cl, K reabsorption

o PT Applicationo Hypotension from hypovolemiao Hypokalemiao Dehydration

DECREASE PRELOAD/AFTERLOAD

Evidence 5

o Diuretics are recommended in patients with HFrEF who have evidence of fluid retention, unless contraindicated, to improve symptoms. (LOE C. Class I)

oDiuretics should be used for relief of symptoms due to volume overload in patients with HFpEF. (LOE C. Class I)

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Case Update10/19

o Mr. Shock complained of worsening SOB at rest, requiring increasing oxygen. Report of poor UOP x24 hours. Increasing BLE edema noted per medical exam.

o Patient admitted from telemetry floor to cardiac care unit (CCU).

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Physical Exam

DECOMPENSATED HEART FAILURE

o Vitals: Narrow pulse pressure. Hypotensive and +/‐ tachycardia

o Lungs: Rhonchi and rales

o Heart: + S3. +JVD

o Extremities: Cold and edematous

o Neuro: +/‐ Confusion

o Kidneys: Decreased UOP

MR. SHOCK 10/19

oVitals: BP 86/52 mmHg. HR 110

oLungs: Coarse rales throughout

o Heart: + S3. +JVD

o Extremities: Cold, 2+ pitting edema in BLE up to hips

o Neuro: Mild altered mental status

o Kidneys: < 250 ml UOP in past 24 hours

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Heart Failure

1


No Yes

NoWarmDry

WarmWet

YesCold Dry

Cold Wet

Eviden

ce of Low Output

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No Yes

NoWarmDry

WarmWet

YesCold Dry

ColdWet

Eviden

ce of Low Output

Case Update10/19

o In CCU, invasive hemodynamic lines were placed:o Central lineo Swan‐Ganz Cathetero Arterial line

o Pt on 10 L high flow cannula.

Central LineoCentral Venous Pressure (CVP)

oBlood return to right atrium

oIndication of volume status

oScvO2oOxygen saturation of venous blood, from SVC only

oIndirect measure of heart function

oNormal 60‐80%

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Swan‐Ganz Catheter(SGC)

o Pulmonary Artery Pressure (PAP)o Cardiac Output (CO)o Cardiac Index (CI)

o CO/BSAo Systemic Vascular Resistance (SVR)

o Afterloado SvO2

o Mixed venous oxygen saturationo SVC + IVC = Whole body oxygen consumption

o 60‐80 mmHg

Cardiogenic Shock (CGS)

o Clinical condition of inadequate tissue (end organ) perfusion due to cardiac dysfunction o Hypotension (SBP < 80‐90 mmHg) or MAP 30 mmHg below baseline

o Reduced cardiac index <1.8 L/min/m2 without support, or <2.0‐2.2 L/min/m2 with support

o Elevated “filling pressures”

Normal value8 Patient value

Blood Pressure 100‐140/60‐90 mmHg 86/52 mmHg

Heart Rate 60‐100 bpm 110 bpm

SpO2 >92% 93%

Respiratory Rate 12‐20 bpm 29 bpm

Pulmonary Artery Press.(PAP) 15‐30/8‐15 mmHg 42/25 mmHg

Central Venous Pressure (CVP) 2‐6 mmHg 23 mmHg

Cardiac Output (CO) 4‐8 L/min 3.9 L/min

Cardiac Index (CI) 2.5‐4 L/min/m2 1.7 L/min/m2

Systemic Vasc Resistance(SVR) 800‐1200 dynes‐sec/cm5 1419 dynes‐sec/cm5

Mixed Venous Saturation (SvO2) 60‐80% 43%

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Cardiogenic Shock

Medical Management

Inotropes/Pressors

Mechanical Circulatory Support

IABP ECMO

Cardiogenic Shock

Medical Management

Inotropes/Pressors


IABP ECMO

Pharmacological support for CGS

Inotropes Milrinone Increase contractility

Decrease afterload

Dobutamine Increase contractility

Decrease afterload

Dopamine (5‐10) Increase contractility

Dopamine (10‐20) Increase contractility

Increase afterload

Epinephrine (<0.2) Increase contractility

Decrease afterload

Epinephrine (>0.2) Increase afterload

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Pharmacological support for CGS

Vasopressors Norepinephrine Increase afterload

Vasopressin Increase afterload

Phenylephrine Increase afterload

Case Update10/20

o Mr. Shock was started on 0.375 mcg/kg/min of milrinone, remains on diuretics drip.

o He complained of discomfort from lying in bed, and generalized fatigue.

o PT consult placed

Normal value8 Patient value



SpO2 >92% 95%



Central Venous Pressure (CVP) 2‐6 mmHg 20 mmHg





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Exercise Training in Heart Failure

o Exercise training (or regular physical activity) is recommended as safe and effective for patients with HF who are able to participate to improve functional status. (LOE A. Class I) 5

Exercise Training in Heart Failure

o Exercise training (or regular physical activity) is recommended as safe and effective for patients with HF who are able to participate to improve functional status. (LOE A. Class I) 5

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Hemodynamics of Cold

BP: 95/52 mmHg

CI: 2.1 L/min/m2

SvO2: 53%

Hemodynamics of Wet

CVP: 20 mmHg

Hemodynamics of PT TreatmentoExercise/Stress Intolerance

o BPo HRo SpO2 o RRo PA Pressureso CVPo SvO2/ScvO2 o Symptoms: SOB, dizziness, fatigue/weakness

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Defining the Undefined in End‐Stage Heart Failure

PT role in medical

management

PT role in medical

management

• More inotropic support?

• More/less BP support?

• More/less volume removal?

Objective assessmentsObjective

assessments

• 6 MWT

• 5x chair rise

• SPPB

References (Slides 1‐59)1. Ruhela, Manish. (2014). 2013 ACCF/AHA Guidelines for the Management of Heart Failure [PowerPoint Slides]. Retrieved from

https://www.slideshare.net/manishdmcardio/chf‐guidelines‐2013seminar

2. Klabunde, R.E. (2007) Preload (Image). Retrieved from http://cvphysiology.com/Cardiac%20Function/CF007

3. Klabunde, R.E. (2007) Afterload (Image). Retrieved from http://cvphysiology.com/Cardiac%20Function/CF008

4. Klabunde, R.E. (2007) Inotropy (Image). Retrieved from http://cvphysiology.com/Cardiac%20Function/CF010

5. Goff DC Jr., Lloyd‐Jones DM, Bennett G, Coady S, D’Agostino RB, Gibbons R, Greenland P, Lackland DT, Levy D, O’Donnell CJ, Robinson JG, Schwartz JS, Shero ST, Smith SC Jr., Sorlie P, Stone NJ, Wilson PW, Jordan HS, Nevo L, Wnek J, Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH, DeMets D, Hochman JS, Kovacs RJ, Ohman EM, Pressler SJ, Sellke FW, Shen WK, Smith SC Jr., Tomaselli GF; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2013 ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129(25 suppl 2):S49–S73. doi: 10.1161/01.cir.0000437741.48606.98.

6. Klabunde, R.E. (2007) Cardiac Output Curve (Image). Retrieved from http://www.cvphysiology.com/Cardiac%20Function/CF027

7. Klabunde, R.E. (2007) Diuretics (Image). Retrieved from http://cvpharmacology.com/diuretic/diuretics

8. McGee WT, Headley JM, Frazier JA. Quick Guide to Cardiopulmonary Care. 3rd ed. Edwards Lifesciences Corporation; 2014

Case update 10/22

o The patient is on inotropic support.o In his current state of volume overload, the patient has

demonstrated decreased oxygenation.

o Clinical presentation:o SpO2 88‐90% at resto He is unable to lie flat and is unable to complete full

sentences without SOBo His resting RR is in the 40’s

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Oxyhemoglobin Curve

Case update continued

o Pertinent lab values to evaluate oxygenation:o ABG: 7.30/40/55/28o SvO2: 51%

o Placed on NIPPV

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What are our options for providing supplemental oxygen to patients?

Non‐invasive forms of

oxygenation/ventilation

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Case Update10/23

o Patient failed NIPPV

oIntubated and placed on volume control ventilationoRR 20

oTidal Volume 450 ml

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Mechanical (Invasive) Ventilation

Basics of Positive Pressure Ventilation (PPV)

The “Who”

The “What”

The “Why”

Indications for Positive Pressure Ventilation (PPV)1

Invasive PPV

Protection of unstable airway

Decreased risk of aspiration

Facilitate procedures (i.e. bronchoscopy)

Non‐invasive and Invasive PPV

Increased work of breathing

•Reduce work of breathing

•Prevent muscle fatigue or speed muscle recovery

Poor gas exchange

•Allow adequate alveolar ventilation (PEEP)

Assist in correction of hypoxemia (FiO2)

•Allow higher concentration of oxygen delivery

•Reduce shunting by maintaining open alveoli

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Volume Ventilation(CMV, AC/VC)

Set variables

Rate

Tidal Volume

Dependent variables

Airway Pressure

��

Pressure Ventilation(pressure control)

Set variables

Rate

Airway pressure

Dependent variables

Tidal volume

Can this patient benefit from PT intervention?

oEarly evidenceoImproved hospital and patient outcomes

‐ use of sedation 2,3

‐ delirium 2,3

‐ ICU & hospital stay 2,3

oVentilated patients: ‐ delirium 4

o Improved functional outcomes at hospital discharge 4

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Can this patient benefit from PT intervention?

oCurrent evidenceoImproved hospital and patient outcomes5

o financial burden on hospitals5

oVentilated patients:6

o mechanical ventilator dayso ICU length of stay

What happens at Piedmont Hospital?

oMechanical ventilation order set

oSedation awakening trial

oSpontaneous breathing trial

oPT consult

Mechanical Ventilator Weaning:Sedation Awakening Trial (SAT)

Elevated intracranial pressure

Active myocardial infarction

Paralytics

Agitation

Alcohol Withdrawal

Active Seizures

Prone position

Newly intubated/terminal extubation

Therapeutic Hypothermia

Scheduled A.M. procedure

Open chest/abdomen

Elevated intracranial pressureExclusion

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Mechanical Ventilator Weaning: Spontaneous Breathing Trial

pH greater than 7.25

FiO2 less than or equal to 50%

PEEP less than or equal to 7.5 cmH2O

PaO2 greater than 60 or O2 saturation greater than 88%

RASS at target or sedation off for a minimum of 2 hours

Inclusion

MAP >/= 65 mmHg on low dose vasopressors

RR less than 30 bpm

RSBI less than 105

NIF greater than ‐20

Minute Ventilation 5‐15 L/min

Mechanical Ventilation PT Order SetWHAT IS THE ROLE OF PT PAH ORDER SET

o No active bleedingo Heart rate 60‐120 bpmo Mean Arterial Pressure

(MAP) > 60 mmHgo No new or increased vasopressor

requirements within 2 hourso SpO2 > 88%o Respiratory rate < 30o FIO2 < 60%o PEEP < 10 cm H2Oo RASS greater than ‐3

PT Treatment SessionVital Signs Before

HR 105

BP 114/62

SpO2 97

RR 20

Tidal Volume (Vt) 450

Airway Pressure 24 cm H20

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PT Treatment SessionVital Signs Before During

HR 105 123

BP 114/62 94/52

SpO2 97 96

RR 20 28

Tidal Volume (Vt) 450 450

Airway Pressure 24 cm H20 48

Hemodynamic Considerations

Positive Airway Pressure

Lung Volumes

CompressesHeart

Decreases Preload

Decreases Cardiac Output

Clinical: SBT during PT

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Pulmonary Toileting/Hygiene

Assisted coughing techniquesAssisted coughing techniques

Chest PT Chest PT

Deep suctioningDeep suctioning

Postural drainagePostural drainage

TH [2]1

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Postural Drainage

TH [2]1 Should this be dark and light for effect?Tiffany Haney, 12/14/2017

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Methods of Mobilization

12

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Barriers to Early Mobility

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References (Slides 61‐85)1. Broccard MD, A & Marini MD, J. Basics of Mechanical Ventilation. Society of Critical Care Medicine.

February 15, 2008.

2. Corcoran J, Herbsman J, Bushnik T, et al: Early rehabilitation in the medical and surgical intensive care units for patients with and without mechanical ventilation: an interprofessional performance improvement project. PMR J. 2017; 9: 113‐9.

3. Engel HJ, Tatebe S, Alonzo PB, et al: Physical therapist‐established intensive care unit early mobilization program: a quality improvement project for critical care at the University of California San Francisco Medical Center. Phys Ther. 2013; 93: 975‐985.

4. Lai C‐C, Chou W, Chan K‐S et al: Early mobilization reduces duration of mechanical ventilation and intensive care unit stay in patients with acute respiratory failure: a quality improvement project. Arch Phys Med Rehabil. 2017; 98: 931‐9.

5. Needham D, Korupolu R, Zanni J, et al: Early physical medicine and rehabilitation for patients with acute respiratory failure: a quality improvement project. Arch Phys Med Rehabi. 2010; 91: 536‐542.

6. Schweickert WD, Pohiman MC, Pohiman AS, et al: Early physical and occupational therapy in mechanically ventilated, critically ill patients: A randomized controlled trial. Lancet. 2009; 373: 1874‐188

1 ADD PICTURESTiffany Haney, 12/11/2017

2 Remove if pictures addedTiffany Haney, 12/11/2017

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Case update 10/26

o Mr. Shock has successfully extubated. Supported on 4 L NC.o The heart failure team has deemed the patient appropriate

for ASO this admission, and will discuss LVAD vs OHT.o However, based on borderline hemodynamics, the HF has

decided to support the patient with mechanical circulatory support

Cardiogenic Shock

Medical Management

Inotropes/Pressors


IABP ECMO

Cardiogenic Shock

Medical Management

Inotropes/Pressors


IABP ECMO

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Background: Intra‐aortic Balloon Pumps (IABPs)

o What?o Mechanical circulatory

support device consisting of a console and catheter with balloon at the distal end1


o Where?o Balloon resides in the

proximal descending aorta. Insertion site varies, primarily femoral1


o How?o Diastolic augmentation of

blood pressure with balloon inflation(Helium). Deflation of balloon in systole1

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o Why?o Improves coronary

perfusion during diastolic inflation2


o Why?o Improves coronary perfusion

during diastolic inflation

o Decreases afterload/improves cardiac output with systolic deflation.2


o Severe Coronary Disease

o Angina refractory to max medical management

o Acute cardiogenic shocko Advanced CHF awaiting

ASO who fail single/dual inotropic support2

Who?

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Background: Complications

Major

Minor

• Dissection

• IABP Rupture

• Major ischemia

• Major bleeding

• Major migration• IABP malfunction

• IABP Migration

• Minor bleeding

• Thrombocytopeniaia

Background: Complications of IABPs

o Estimated 70,000 IABPs inserted annually with documented incidence between 5‐10%

o 8‐18% angioischemic complications.o Major limb ischemia 1%4

o Over 240 institutions: 7% total complication rate associated with an IABP

o Nearly 3% rate of major complications and a mortality rate of 0.5% directly associated to an IABP5

Background: Physical therapy involvement

• 18 CHF patients with axillary IABPs as BTT• Ambulated regularly

• Infection (0%)• IABP replacement (16.7%)

• IABP failure (5.6%)• IABP migration (5.6%)• IABP kinking (5.6%)

• None with ambulation

AxillaryVanderbilt Heart Institute6

• 88 CHF patients with SC IABPs as BTT• 84 ambulated up to 3x/day• 16 participated in early mobility

• 29% IABP exchange/reposition• 1.1% thrombosis• 4.5% hematoma• 2.3% infection

SubclavianUniversity of Chicago Medicine7

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Background: Physical therapy involvement

o Femoral insertion site:

o Bed mobility, strengthening/ROM of extremities without IABP

o NO standing upright. NO Ambulation.

o Hospital specific guidelines on hip flexion restrictions.

o <30 degrees

Proposed Guidelines for Safe Ambulation of Patients with Femoral IABP in Cardiac Care Unit

Order to ambulate must be approved by the provider on service in the CCUPerfusion must be notified if ambulating patient with femoral IABP

IABP must be sutured to the leg at insertion site and secured distally

Patient must currently be chest pain free

Patient must have on non-skid socks

Saturations by pulse oximetry measuring 92% or greater at resting

Patient demonstrates ability to stand and weight bear with adequate BLE strength with or without an assistive device

Physical therapist must be present to ambulate patient and must have tilt table to facilitate standing of patient while avoiding flexion of hips

Patient must be returned to bed immediately if:

Becomes orthostatic/nauseated

IABP becomes dislodged or insertion site starts to bleed

Complains of chest pain

Hypotensive blood pressure response to activity or heart rhythm changes that lead to hemodynamic instability

Signs of ischemia/evidence of migration of IABPRepeat CXR after ambulation if concerned that IABP is still in adequate position

If concern about IABP functioning physician/surgeon must be notified immediately

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What We Do at Piedmont!

o 122 Physical therapy sessions

o 78 Ambulation

o 44 Other

o Tilt only (19)

o Tilt with exercise (25)

o Marching

o Mini‐squats

o Toe presses

o Hip abd/adduction

Minor Complications

o Minor bleed at insertion site 0/78

o Hematoma 0/78

o IABP migration (without hemodynamic compromise) 0/78

o Paresthesia 0/78

o Lower Extremity 0

o Upper Extremity 0

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Major Complication

o Vascular Compromise 0/78

o Arterial Dissection 0

o Aorta 0

o Iliac 0

o Femoral 0

Major Complication

o Limb Ischemia 0/78

o Aneurysm 0/78

o Aorta 0

o Iliac 0

o Femoral 0

Major Complication

o IABP Malfunction 0/78

o Rupture 0

o Kinking 0

o Migration 0

o Myocardial Infarction 0/78

o Mobility‐related CVA 0/78

o Mobility‐related death 0/78

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o Ambulating patients with femoral IABPs in situ is a safe treatment options using specific guidelines and multi‐disciplinary team

References (Slides 87‐108)1. Peura JL, Colvin‐Adams M, Francis GS, et al. Recommendations for the use of mechanical circulatory support:

device strategies and patient selection: a scientific statement from the American Heart Association. Circulation. 2012;126(22):2648‐2667.

2. Davidson J, Baumgariner F, Omari B, Milliken J. Intra‐aortic balloon pump: indications and complications. J Natl Med Assoc. 1998;90(3):137‐140.

3. Ferguson J, Cohen M, Freedman R, Stone G, Joseph D, et al: The current practice of intra‐aortic balloon counterpulsation: results from the Benchmark Registry. J Am Coll Cardiol 2001, 38:1456‐1462

4. Parissis H, Soo A, Al‐Alao B. Intra aortic balloon pump: literature review of risk factors related to complications of the intraaortic balloon pump. J Cardiothorac Surg. 2011;6:147.

5. Macauley K. Physical therapy management of two patients with stage d heart failure in the cardiac medical intensive care unit. Cardiopulm Phys Ther J. 2012;23(3):37‐45.

6. Umakanthan R, J, Solenkova N, et al. Benefits of ambulatory axillary intra‐aortic balloon pump for circulatory support as bridge to heart transplant. J Thorac Cardiovasc Surg. 2012;143(5):1193‐1197.

7. Tanaka A, Tuladhar SM, Onsager D, et al. The Subclavian Intraaortic Balloon Pump: A Compelling Bridge Device for Advanced Heart Failure. Ann Thorac Surg. 2015;100(6):2151‐2157; discussion 2157‐2158.

Case Update11/2

o Mr. Shock participated in daily sessions of ambulation with IABP in situ.

o However, on 11/2, he began demonstrating signs of active infection.

o Decision by the medical team to remove IABP as possible source of infection with the addition of Dobutamine

o Infection treated empiricallyo After 5‐7, No growth on blood cultures and clinical symptoms

of infection resolve (i.e. normotensive, decrease in WBC, down trend of LA)

o Hemodynamically, he continues to demonstrate marginal CI/CO despite dual inotropic support. SCr continues to slowly increase.

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Normal value Patient value



SpO2 >92% 90%



Central Venous Pressure (CVP) 0‐8mmHg 15 mmHg





Clinical Presentation

Cold # ��

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Case update cont. 11/3

o Patient demonstrates progressive SOB and fatigue. Medical team decides to increase his support.

Cardiogenic Shock

Medical Management

Inotropes/Pressors


IABP ECMO

Cardiogenic Shock

Medical Management

Inotropes/Pressors


IABP ECMO

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Extracorporeal Membrane Oxygenation (ECMO)

•Artificial cardiac and/or pulmonary support

What?

2


• Critically ill patients who are unable to be adequately supported from cardiac and/or pulmonary standpoint through conventional medical interventions.

Who?

2


• Critically ill patients who are unable to be adequately supported from cardiac and/or pulmonary standpoint through conventional medical interventions.

How?

2

2 I need to site indication from articles at workErica Colclough, 12/11/2017

Slide 122


Slide 123


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ECMO Configuration

TRADITIONAL

Venovenous (VV)‐pulmonary support

Venoarterial (VA)‐cardiac support

“HYBRIDS”

RVAD

VA ‐V

VV‐A

RA‐LA DRAIN

Percutaneous LVAD

Veno‐Arterial ECMO

o Inability to provide adequately oxygenated blood to peripheral circulation for tissue perfusion

o Continued/worsening shock

o Despite inotropic, and/or vasopressor support

o Despite IABP or Impella

Why?

Veno‐Arterial ECMO

o CannulationoCentral

oPeripheral

o AccessoDrain: Venous

oReturn: Arterial

How?

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VA ECMO Peripheral CannulationPERIPHERAL CANNULATION

VA ECMO Central CannulationCENTRAL CANNULATION

Superficial Femoral Artery (SFA)

• Provides arterial blood flow to the cannulated lower extremity

Why?

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Superficial Femoral Artery (SFA)

• Access:

• Drain: Arterial cannula of circuit

• Return: superficial femoral atery

How?

Veno‐Venous ECMO

o ARDS brought on by pneumonia, flu, or other disease processes

o Severe asthma with bronchospasm

o Refractory hypoxemia or hypercapnia despite optimal ventilation

WHY?

Veno‐Venous ECMO

o CannulationoCentral

o Peripheral

o AccessoDrain: Venous

oReturn: Venous

How?

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VV ECMO Peripheral Cannulation

VV ECMO Central Cannulation

oNon‐pulsatile flow

o Increased afterload

oDecreased preload

oVenous blood to the lungs

oMicroemboli to the body

oDirect cardiac support

oArterial saturation 95‐100%

o “Comfortable” for the staff

VA

ECMO

VA

ECMO

o Pulsatile flow

oNo change in afterload

oNo change in preload

oOxygenated blood to the lungs

oMicroemboli to the lungs

o Indirect cardiac support

oArterial saturation 80‐95%

o “Concerning” for staff

VV

ECMO

VV

ECMO

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The Control Panel

oLiters Flow (Lpm)

oRevolutions Per Minute (RPM)

The Blender/Flow Meter

Spectrum Monitor

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The Pressure MonitorP1 PRESSURE

The pressure generated in order to pull the blood into the pump

P2 PRESSURE

The pressure the pump pushes against to return blood back to the body

The Oxygenator

The Pump

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The Hand Crank

Case Update 11/15

o Mr. Shock is cannulated for VA ECMOo Drain: Left FVo Return: Right FA, with SFA

o Flow 4.5 L, RPM 2985, Sweep 8 L/min, FiO2 100%

o Off all vasoactive dripso 6 L NCo PT consult for mobility

Now What?!

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Mobility Criteria For ECMO Patients

What Does The Literature Say?

Evaluation Of Patient Hemodynamic/Pulmonary Status

Clear Understanding Of How The Circuit Is Supporting The Patient

What Happens at Piedmont Hospital?

ECMO Coordinator

ICU Intensivist

Cannulating MD

Perfusion

Bedside RN

Rehab Services

Respiratory therapy (as indicated with management of artificial airway)

Monitoring/Assessment For Mobilization

Vital signs

Subjective report

Auscultation

Vascular status of cannulated limb

Blood gas (ABG)

Imaging/lab

Peripheral edema

Cognition

Oxygenator blood gas

Cannulation site

Integrity/positioning of ECMO cannulas/SFA

ECMO circuit flow

ECMO circuit P1/P2

Sweep

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Inspect/Secure The Cannulation Site

Circuit Assessment

o Ensure circuit is free of anything lying on or interfering with flow

oNo Tangles! Try to prevent them before they occur!

oLines off the floor → DANGEROUS!

oGas Hoses → Yellow & Green → Ensure Patency

o Prevent kinking

o Blender will alarm

oQuadrox Oxygenator should be perpendicular to foot board

oSorin Pump Head should be below cannulation site

Interventions

oFunctional MobilityoCardiovascular/Pulmonary

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Functional MobilityoBed mobilityoTransfer TrainingoGaitoBalanceoCoordinationoStrength training

Cardiovascular/PulmonaryoPostural assessmentoBreathing mechanics oInspiratory muscle trng.oAerobic training

Response to Therapy SessionHEMODYNAMICS

Goal: Warm

Ensure good forward flow/oxygen delivery

oECMO

oMaintain adequate flows

oMonitor SvO2 per circuit

oPatient

oNative cardiac function remains stable/normal hemodynamic response to mobilization.

PULMONARY

Goal: Dry

Ensure stable pulmonary status (oxgyentation/ventilation)oECMO

oMonitor for competitive flow

oMonitor color change of cannulas

oPatient

oMonitor vs for respiratory status

oAuscultation

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Clinical Questions On The Horizono Can ECMO parameters be adjusted during mobilization activity to optimize

participation with therapy (i.e. sweep, flow, FiO2)?

o Ability/Role of PT in the titration of ECMO support with therapy?

o Role of PT in candidacy for decannulation?

o Implications of participation with mobilization for vascular repair at time of decannulation?

Mobilization Results

CONFIGURATION OF ECMO

TOTAL NUMBER OF PATIENTS MOBILIZED

TOTAL NUMBER OF MOBILIZATION

SESSIONS

TOTAL NUMBER OF ADVERSE OUTCOMES

VA ECMO: FEMORAL CANNULATION 11 34 0

VV ECMO:FEMORAL CANNULATION 12

360

VV ECMO: AVALON CATHETER 26 138 0

RVAD: 29 F PROTEK CATHETER

125

0

RVAD: CENTRAL CANNULATION 1 5 0

VA‐V 3 12 0

VV‐A (TRANSEPTAL)

1 4 0

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Case Update 11/25

o Mr. Shock was weaned off vasopressors and remains only on milrinone for support

o Supplemental oxygen 2l/min via nco Improving chest x‐ray/intermittent medical pharmacological

diuresiso Improving lab values to suggest better organ perfusiono OOB to chair and ambulating with physical therapy while

support on VA ECMO x5 week

Advanced Surgical Options Evaluation SURGICAL EVALUATION OPTIONS

Heart Transplantation

Left ventricular assist device (LVAD)o Bridge to transplantation

o Destination therapy

EVALUATION TEAM

Cardiology

Cardiothoracic surgery

Social worker/Case manager

Spiritual/Palliative care

LVAD pre‐op Education‐LVAD coordinator

Physical Therapy

Functional Pre‐op Frailty Evaluation SUBJECTIVE REPORT

Kansas City Cardiomyopathy Questionnaire (KCCQ)

OBJECTIVE ASSESSMENT

Short Physical Performance Battery(SPPB)

oBalance

oFunctional Lower Extremity Strength

oGait Speed

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References (Slides 110 ‐153)

QUESTIONS?

defining the undefined in critical rehabilitation · defining the undefined in critical care...

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