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CRRT: It

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During the course of her stay in MICU, she developed AKI. To manage her fluid and electrolytes, she was started on CRRT. She seemed to tolerate CRRT well. – PowerPoint PPT presentation

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Title: CRRT: It


1
CRRT Its Not Just for Renal Failure Anymore
  • Presented by
  • Sue Fallone,MS,RN,CNN
  • Clinical Nurse Specialist
  • Adult and Pediatric Dialysis
  • Albany Medical Center

2
Objectives
  • Define Heart Failure
  • Define Sepsis
  • Discuss medical management of heart failure and
    sepsis
  • Describe indications for CRRT for these disorders
  • Case Study

3
HEART FAILURE
Clinical syndrome that can result from any
structural or functional cardiac disorder that
impairs the ability of the ventricle to fill with
or eject blood
4
Incidence of Heart Failure
  • More deaths from heart failure than from all
    forms of cancer
  • Nearly 1 millions people are admitted to the
    hospital with CHF and 30-60 are readmitted
  • Contributed to 53,000 deaths in the U.S. each
    year
  • About 550,000 new cases per year
  • Affects men and women equally
  • Related to the aging population, lower death rate
    from MI, and improved treatment for heart disease
  • http//health.usnews.com/health-conditions/heart-
    health/congestive-heart

5
Causes of Heart Failure
  • Main causes
  • Ischemic heart disease, Cardiomyopathy,
    Hypertension, Diabetes
  • Other causes Valvular heart disease, Congenital
    heart
  • disease, Alcohol and drugs, Hyperdynamic
    circulation
  • (anemia, thyrotoxicosis, hemochromatosis, Paget's
  • disease), Right heart failure (RV infarct,
    pulmonary
  • hypertension, pulmonary embolism, cor pulmonale
  • (COPD)), Arrhythmia and Pericardial disease.

6
Mechanisms Leading to Heart Failure
  • Impaired cardiac contractility as in myocardial
    infarction and cardiomyopathy
  • Ventricular outflow obstruction (pressure
    overload) as in hypertension and aortic stenosis
  • Impaired ventricular fillings as in mitral
    stenosis and constrictive pericarditis
  • Volume overload as in mitral regurgitation

7
Precipitating Factors
  • Infections
  • Arrhythmias
  • Physical, Dietary, Fluid, Environmental, and
    Emotional Excesses.
  • Myocardial infarction
  • Pulmonary embolism
  • Anemia
  • Thyrotoxicosis and pregnancy
  • Aggravation of hypertension
  • Rheumatic, Viral, and Other Forms of Myocarditis
  • Infective endocarditis
  • Diabetes

8
Cardiac remodeling
? C.O.P
  1. Hypertrophy Dilatation

2. ?Sympathetic activity
  • ? H.R.
  • V.C

?
  • ? E.D.V

? After-load
? Pre-load.
Angiotensin
Na water retention
?
Aldosterone
9
TYPES OF HEART FAILURE
  • Left- sided or left ventricular (LV) heart
    failure
  • is commonly caused by ischemic heart disease but
    can also occur with valvular heart disease and
    hypertension. 2 types of (LV) heart failure
  • diastolic failure is a syndrome consisting of
    symptoms and signs of heart failure with
    preserved left ventricular ejection fraction
    above 4550 and abnormal left ventricular
    relaxation assessed by echocardiography
  • systolic failure is when the left ventricle loses
    its ability to contract normally, can pump
    enough blood into the systemic circulation
  • Right-sided or right ventricular (RV)heart
    failure
  • may be secondary to chronic( LV ) heart failure
    but can occur with primary and secondary
    pulmonary hypertension, right ventricular
    infarction.

10
TYPES of HEART FAILURE
  • Congestive Heart Failure-
  • Blood flow out of the heart slows, blood
    returning to the heart through the veins backs up
    and congestion in the bodys tissues
  • Will see edema, SOB, can affect kidney function

11
Symptoms Signs OF Heart Failure
  • Left heart failure
  • Symptoms are predominantly fatigue,
  • exertional dyspnea, orthopnea and PND
  • Physical signs Cardiomegaly, gallop
  • functional mitral regurgitation and crackles a
    the lung bases.

12
  • Right Heart Failure
  • Symptoms (fatigue, breathlessness, anorexia and
    nausea) relate to distension and fluid
    accumulation in areas drained by the systemic
    veins.
  • Physical signs are usually more prominent than
    the symptoms, with
  • jugular venous distension
  • tender smooth hepatic enlargement
  • dependent pitting edema
  • development of free abdominal fluid (ascites)
  • Pleural effusion (commonly right-sided).
  • Dilatation of the right ventricle produces
    cardiomegaly and may give rise to functional
    tricuspid regurgitation. Tachycardia and a right
    ventricular third heart sound are usual.

13
Major symptoms signs of heart failure
14
Classification of Heart FailureFunctional
Capacity
  • Class I patients with cardiac disease and no
    limitation of physical activity
  • Class II- patients with cardiac disease slight
    limitation of physical activity results in
    fatigue, palpitation, dyspnea or angina
  • Class III-patients with cardiac disease marked
    limitation of physical activity comfortable at
    rest
  • Class IV-patients with cardiac disease inability
    to carry on any physical activity, symptoms of
    heart failure at rest
  • http//www.heartorg/HEARTORG/
    Conditions/Heart

15
Treatment of heart failure
? C.O.P
Positive Inotropics
2. ?Sympathetic activity
  1. Hypertrophy Dilatation
  • ? H.R.
  • V.C

?
? Pre-load.
  • ? E.D.V

? After-load
vasodilators
Angiotensin
ACE inhibitors
Diuretics
Na water retention
?
Aldosterone
16
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17
If Resistant to Diuretics
  • MAY NEED
  • Ultrafiltration

18
UNLOAD STUDY
  • The UNLOAD study was a randomized, multicenter
    study of 200 patients involving 28 hospitals and
    medical centers across the United States. UNLOAD
    compared the short and long-term safety and
    efficacy of an advanced form of ultrafiltration
    therapy(Aquapheresis) to the use of conventional
    diuretic drug therapy in fluid overloaded heart
    failure patients.
  • The UNLOAD study was published in the February
    13, 2007 issue of Journal of American College of
    Cardiology. (Costanzo MR et al. JACC 2007
    49(6)675-683).

19
UNLOAD StudyResults
  • 28 with greater fluid loss with UF
  • 43 reduction in patients being
    re-hospitalization for HF
  • 63 fewer hospital days for HF

20
What is SIRS?
  • The systemic inflammatory response syndrome is
    systemic level of acute inflammation, that may or
    may not be due to infection, and is generally
    manifested as a combination of vital sign
    abnormalities including fever or hypothermia,
    tachycardia, and tachypnea.

21
Definitions
  • Severe SIRS SIRS in which at least 1 major
    organ system has failed.
  • Sepsis SIRS which is secondary to infection.
  • Severe Sepsis Severe SIRS which is secondary to
    infection.
  • Septic Shock Severe sepsis resulting in
    hypotensive cardiovascular failure.

22
Systemic Inflammatory Reponse(SIRS)
  • Can be triggered by infectious and
    non-infectious events
  • Infectious causes bacteria or fungi
  • Non infectious causes are prancreatitis,burns,
    trauma
  • SIRS is the term used for noninfectious causes

23
Criteria for SIRS
  • Requires 2 of the following 4 features to be
    present
  • Temp gt38.3 or lt36.0 C
  • Tachypnea (RRgt20 or MVgt10L)
  • Tachycardia (HRgt90, in the absence of intrinsic
    heart disease)
  • WBC gt 10,000/mm3 or lt4,000/mm3 or
  • gt10 band forms on differential

24
Criteria for Severe SIRS
  • Must meet criteria for SIRS, plus 1 of the
    following
  • Altered mental status
  • SBPlt90mmHg or fall of gt40mmHg from baseline
  • Impaired gas exchange
  • Metabolic acidosis (pHlt7.30 lactate gt 1.5 x
    upper limit of normal)
  • Oliguria (lt0.5mL/kg/hr) or renal failure
  • Hyperbilirubinemia
  • Coagulopathy (platelets lt 80,000-100,000/mm3,
    INR gt2.0, PTT gt1.5 x control, or elevated fibrin
    degredation products)

25
Pathophysiology of Sepsis
  • Overwhelming inflammatory response
  • Increased production of proimflamatory cytokines
    and decreased production of cytokines( which
    inhibit inflammation)
  • Clotting cascade activated
  • Peripheral Vasodilatation ? systemic vascular
    resistance

26
Pathophysiology of Sepsiscontinued
  • C/O decreases
  • Intravascular fluid loss
  • Decreased pre load-hypotension
  • ATN-renal hypoperfusion and ischemic injury
  • MODS
  • MOF

27
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28
Relationship Between SIRS and Sepsis
Adapted from Marini JJ, et al. Critical Care
Medicine, 2nd ed. 1997.
29
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30
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31
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32
Risk Factors for SIRS/Sepsis
  • Age
  • Indwelling lines/catheters
  • Immunocompromised states
  • Malnutrition
  • Alcoholism
  • Malignancy
  • Diabetes
  • Cirrhosis
  • Male sex
  • Genetic predisposition?

33
Prognosis
  • Overall mortality from SIRS/sepsis in the U.S. is
    approximately 20. Mortality is roughly linearly
    related to the number of organ failures, with
    each additional organ failure raising the
    mortality rate by 15.
  • Hypothermia is one of the worst prognostic signs.
    Patients presenting with SIRS and hypothermia
    have an overall mortality of 80.

34
Treatment
  • Fluid Resuscitation
  • Vasopressors
  • Antibiotics
  • Eradication of infection
  • Ventilatory support, activated protein C,
    steroids, glycemic control, nutrition
  • CRRT

35
CONTINUOUS RENAL REPLACMENT THERAPY
36
CRRT Definition
  • CRRT Continuous Renal Replacement Therapy
  • Defined as
  • Any extracorporeal blood purification therapy
    intended to substitute for impaired renal
    function over an extended period of time and
    applied for or aimed at being applied for 24
    hours /day.
  • Bellomo R., Ronco C., Mehta R,Nomenclature for
    Continuous Renal Replacement Therapies,AJKD, Vol
    28, No. 5, Suppl 3, November 1996

37
Introduction to CRRT
  • Why continuous therapies?
  • Continuous therapies closely mimic the native
    kidney in treating ARF and fluid overload
  • Slow gentle
  • Remove fluid and waste products over time
  • Tolerated well by the hemodynamically unstable
    patient

38
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39
Indications for Therapy
  • Acute kidney injury- preferred in the critically
    ill patient
  • Fluid overload- can removed large amounts of
    fluid slowly
  • Hemodynamically unstable- continuous therapy
    allow for slow hourly fluid removal which allows
    the intravascular spaces to refill

40
Indications continued
  • Highly catabolic patients who need increased
    clearance rates
  • Patients needing large molecular weight
    substances removed
  • Sepsis

41
Molecular Weight
  • SMALL MOLECULES- 0-500 daltons (urea,
    creatinine)
  • MIDDLE MOLECULES- 500-5000 daltons ( vitamin
    B12)
  • LARGE MOLECULES- 5000-50,000 daltons ( heparin,
    Beta 2 drugs)

42
CRRT Modalities
  • SCUF OR ULTRAFILTRATION - Slow Continuous
    UltraFiltration
  • CVVHD - Continuous Veno-Venous HemoDialysis
  • CVVH - Continuous Veno-Venous Hemofiltration
  • CVVHDF Continuous Veno-Venous
    Hemodiafiltration

43
SCUF/Ultrafiltration
  • Primary therapeutic goal
  • Safe management of fluid removal
  • Patient UF rate ranges up to 2 L/Hr
  • No dialysateNo replacement fluids
  • No molecule removal
  • Large fluid removal via ultrafiltration
  • Blood Flow rates 100-200 ml/min

44
SCUF/ULTRAFILTRATION Slow Continuous
UltraFiltration
45
Ultrafiltration
  • Particles move through a semi-permeable membrane
    by use of HYDROSTATIC pressure.
  • The separation of particles from a suspension by
    passage through a filter. The separation is
    accomplished by convective transport.

46
Convection Step 1 Filter Action
Red Cell
Na
K
Na
Na
Na
U
H2O
H2O
U
H2O
Na
Na
U
H2O
Na
Red Cell
K
H2O
H2O
K
H2O
Red Cell
Na
U
U
Na
Na
Na
H2O
U
Red Cell
Na
Na
U
K
K
H2O
H2O
U
K
K
H2O
U
H2O
Na
H2O
Na
Na
U
K
Na
U
K
Red Cell
H2O
K
Na
Na
H2O
Na
U
K
47
Solute Removal by Convection
Convection The movement of solutes with a
water-flow,solvent drag, e.g... the movement
of membrane-permeablesolutes with water across
the semipermeable membrane
48
CVVH Continuous Veno-Venous Hemofiltration
49
Molecular Transport Mechanisms
  • Convection - The movement of solutes with a
    water-flow, solvent drag, the movement of
    membrane-permeable solutes with water across the
    semipermeable membrane

50
Convection Step 1 Filter Action
Red Cell
Na
K
Na
Na
Na
U
H2O
H2O
U
H2O
Na
Na
U
H2O
Na
Red Cell
K
H2O
H2O
K
H2O
Red Cell
Na
U
U
Na
Na
Na
H2O
U
Red Cell
Na
Na
U
K
K
H2O
H2O
U
K
K
H2O
U
H2O
Na
H2O
Na
Na
U
K
Na
U
K
Red Cell
H2O
K
Na
Na
H2O
Na
U
K
51
Solute Removal by Convection
Convection The movement of solutes with a
water-flow,solvent drag, e.g... the movement
of membrane-permeablesolutes with water across
the semipermeable membrane
52
CVVHD - Continuous VV Hemodialysis
  • Primary therapeutic goal
  • Solute removal by diffusion
  • Safe fluid volume management by ultrafiltration
  • Requires Dialysate solution
  • Patient UF rate ranges 2-7 L/24 hours (300
    ml/hr)
  • Dialysate Flow rate 15-45 ml/min (2 L/hr)
  • Blood Flow rate 100-200 ml/min
  • No replacement solution
  • Solute removal determined by Dialysate Flow rate.

53
Diffusion Filter Action
Na
Na
K
Mg
Mg
Na
Na
U
H2O
Na
Na
U
H2O
Na
H2O
Na
U
Na
K
K
Na
U
H2O
K
Na
Mg
H2O
U
Na
U
H2O
H2O
K
U
H2O
K
U
H2O
Mg
Na
Na
U
K
U
H2O
Na
Na
U
H2O
Na
Na
H2O
K
U
K
Na
Na
Mg
K
54
Vascular Access
  • Depending on the device used lumen size matters
  • If using AquaDex FlexFlow Fluid Removal System
    midline catheters can be used
  • If using CRRT devices hemodialysis type catheters
    need to be placed.

55
Catheter Size
  • Adults
  • 12.5 to 14 french
  • Length will vary 16,19,24,cm
  • Femoral placement least preferred
  • Children (weight based)
  • 5 french single catheter 7 fr dual lumen
  • 8 fr dual lumen
  • 10 fr dual lumen
  • 11 fr dual lumen
  • Length
  • 9 cm, 10 cm, 12 cm, 15 cm

56
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57
Case Study 1
  • Mr. G is a 60 year old man with CAD s/p MI and
    PTCA to LAD in 1997, dyslipidemia, and tobacco
    use who called 911 for severe chest pain on
    11/01/10. This pain was similar in nature to his
    previous MI.

58
ECG in the ambulance
59
History
  • In the ambulance en route to the emergency room,
    the patient developed two episodes of ventricular
    fibrillation which both successfully responded to
    DC cardioversion. After arrival to the cath lab,
    the patient developed cardiogenic shock and
    recurrent ventricular fibrillation requiring
    multiple shocks (he was shocked 11 times in the
    cath lab prior to intervention) and intubation
    with mechanical ventilation.

60
Cath Lab Course
  • Coronary angiography showed
  • Totally occluded mid LAD with thrombus
  • Mild diffuse atherosclerosis of left circumflex
    and right coronary arteries
  • Soon after the first injection there was proximal
    propagation of the LAD thrombus which occluded
    the left main coronary artery
  • A wire was passed to the distal LAD and an
    AngioJet thrombectomy device was used which
    re-established flow

61
Cath Lab Course
  • After the Impella device was placed, the patient
    had no further episodes of ventricular
    fibrillation

62
Immediately Post Cath
  • Patient admitted to the CCU on IV Epinephrine,
    Dobutamine, and Dopamine continuous infusions
  • Echocardiogram the next day showed severe
    anterior wall hypokinesis with EF 25
  • The patient was placed on CVVH then on SCUF to
    remove excess fluid

63
Hospital Course
  • Hospital day 3 Impella device was removed
  • Hospital Day 6 Repeat echocardiogram, EF 50-55
  • Hospital Day 8 Extubated, neurologically intact
  • Hospital Day 16 Discharged to home

64
Case Study2
  • Alan is a 20 year old admitted to a cardiology
    unit with CHF and Situs Inversus. He had SOB ,
    anascara, arrythmias. His blood pressure was
    110/60 mm Hg. He has a serum creatinine of 1.5
    mg/dl. He is in need of a pacemaker but first
    needs 10 liters of fluid removed before placement
    of a pacemaker.
  • He is started on furosemide 80 mg every 8 hours
    and metolazone 10mg/d for 2 days. On day three he
    is given mannitol 25 g every eight hours.
  • He is putting out 3L of urine a day but has only
    decreased his net fluid loss by 3 L due to lack
    of adherance to his fluid restriciton

65
Case StudyContinued
  • Because of his need for a pacemaker, the
    decision was made to place the patient on SCUF.
  • After three days of therapy the patient was at
    his dry weight and stable and was able to receive
    his pacemaker
  • Consideration has to be given related to rate of
    fluid removal and his overall renal function
  • Patient was discharged to home with a follow up
    to a nephrologist

66
Case Study3
  • Mrs. D was admitted to MICU for sepsis. She had
    been hypotensive that required vasopressors.
    During the course of her stay in MICU, she
    developed AKI. To manage her fluid and
    electrolytes, she was started on CRRT. She seemed
    to tolerate CRRT well.
  • On her 5th day of therapy, her Serum Creatinine
    was down to 1.2 from 6.9 and her electrolytes
    were stable, her BP was borderline with MAP gt 60
    mmHg and lt 70 mmHg.
  • CRRT was discontinued and only to be restarted
    after 2 days when the patient became hypotensive
    again that regular HD was not possible given her
    hemodynamic parameters.
  • Patient was started on phenylephrine at 200
    mcg/min and nor-epinephrine at 10 mcg/min. On the
    3rd day of the 2nd therapy, the patient had the
    following data

67
Patient Data
Time BP CVP Vasopressor I and O Balance
2/15 2200 125/60 14 Off -100
2/16 0600 110/65 12 Off -250
2/16 1900 73/85 6 ON -1100
2/17 2300 108/55 10 Off -500
68
Questions
  • What happened in this scenario?
  • What should have been considered in setting the
    net fluid removal rate?
  • How would we assess for the intravascular vs
    extra-vascular fluid status?
  • When will be the right time to advocate for
    discontinuance of CRRT?

69
Conclusion
  • CRRT therapies can be applied to many clinical
    situations
  • The patient goals/outcomes can be enhanced with
    early initiation of this therapy

CRRT IS NOT JUST FOR RENAL FAILURE
70
THANK YOU
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