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Critical Care Nurses Association of the Philippines, Inc 2013 CCNAPI Annual Convention

February 21-22, 2013 Diamond Hotel Philippines, Manila

PROGRAM OF ACTIVITIES

DAY 1: Thursday, February 21, 2013 7:00 am - 8:00 am REGISTRATION

8:00 am - 8:30 am OPENING CEREMONY Ribbon Cutting of Scientific Exhibitors HON. CARMENCITA M. ABAQUIN

Chairmam, Board of Nursing Together with the other Members of the Board of Nursing

Doxology and National Anthem MARIA RHONA T. ESTACIO, RN ICU Nurse, The Medical City

Welcome and Opening Remarks FERDINAND P. AGANON, RN, MAN

Over-all Chair, 2013 CCNAPI Annual Convention Acknowledgement of Participants BEDA B. GALICIA, RN

Secretary, Critical Care Nurses Association of the Philippines, Inc. 8:30 am - 9:30 am Introduction of the Keynote Speaker

MARIA ISABELITA C. ROGADO, RN, MAN President, Critical Care Nurses Association of the

Philippine, Inc. Message from the Keynote Speaker NOEL C. CADETE, RN, MAN

National President, Philippine Nurses Association COFFEE BREAK

9:30 am - 10:30 am PLENARY 1: “Rapid Response in Acute Brain Attack” DAIWAI M. OLSON, PhD, RN, CCRN

Associate Professor of Neurology & Neurotherapeutics

Associate Professor of Neurosurgery Staff Nurse, Neurocritical Care Unit University of Texas Southwestern

10:30 am – 11:30 am PLENARY 2: “Interpretation of Dysrhythmias in ACLS” MARIA ISABELITA C. ROGADO, RN, MAN Professor, Arellano University Graduate School of

Nursing 11:30 am -12:30 pm PLENARY 3: “Challenges in Sepsis Management”

DAIWAI M. OLSON, PhD, RN, CCRN

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12:30 pm - 1: 00 pm LUNCH BREAK 1:00 pm -5:00 pm Beyond the Books: Self Directed Learning (Workshop)

Workshop 1 : “Assessment and Management of the Neurological Patient”

Main Preceptor : Ferdinand P. Aganon, RN, MAN Nurse Manager, Critical Care Unit- Nursing Service Dept. The Medical City

Preceptors : Louie Paul Eugenio, RN Sherlline Carillo, RN Celedonia M. Bienes

Speaker : Richmond G.O. Chang, MD, DPBA Sponsor : Biosolutions, Inc.

Workshop 2 : “Early Goal Directed Therapy in Sepsis” Main Preceptor : Beda B. Galicia, RN Assistant Nurse Manger, The Medical City

Preceptors : Charliemagne M. Marinas, RN Raizzah T. Mansoura, RN

John Christian M. Agustin, RN Sponsor : CCNAPI Workshop 3 : “Rapid Interpretation and Management of Dysrhythmias

in ACLS” Main Preceptor : Maria Isabelita C. Rogado, RN, MAN

Preceptors : Marvin S. De La Cruz, RN Mark Gil De De La Rosa, RN Rogelio E. Gayeta, Jr., RN

Sponsor : Hospira Philippines, Inc.

DAY 2: Friday, February 22, 2013 8:00 am - 9:00 am PLENARY 4: “Nuts and Bolts in Neonatal Resuscitation”

WILFREDO R. SANTOS, MD, FPPS, FPSNBMJ President, Philippine Society of Newborn Medicine Neontologist, University of Santo Tomas

9:00 am – 10:00 am PLENARY 5: “Wound Care Assessment and Management” RAMON O. RIBU, MD

Section Head, CTAMS & Wound Care, Philippine Heart Center 10:00 am – 10:15 am COFFEE BREAK 10:15 am – 11:00 am PLENARY 6: “Palliation and Spiritual Care: Phenomenology

Approach in Critical Care” RUDOLF CYMORR KIRBY P. MARTINEZ, MAN, RP-RN, CAA, LMT, CSTP, PhD(c)

Complementary & Alternative Therapy Nurse Practitioner Pain Management Clinician and Staff Nurse

Philippine Children‟s Medical Center

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11:00 am - 12:00 nn PLENARY 7: “Empowerment of Nurses through a Career Progression Program”

MARCO ANTONIO STO. TOMAS, RN, MAN Member, Board of Nursing

Chair, Council for Nursing Advancement, Recognition & Specialization 12:00 nn - 1: 00 pm LUNCHEON SYMPOSIUM (ABBOTT Laboratories)

1:00 pm -5:00 pm Beyond the Books: Self Directed Learning (Workshop) Workshop 4 : “Dynamic of Wound Care: Assessment and Wound Bed Preparation”

Speaker: : Enrique M. Casto, III, MD Main Preceptor : Ferdinand P. Aganon, RN, MAN

Preceptors : Louie Paul Eugenio, RN Sherlline Carillo, RN Celedonia M. Bienes

Sponsor : BBraun Philippines Workshop 5 : “Resuscitation of the Newborn: The Basics”

Main Preceptor : Maria Isabelita C. Rogado, RN, MAN : Florentina Uy-TY, MD Preceptors : Marvin S. De La Cruz, RN

Mark Gil De De La Rosa, RN Rogelio E. Gayeta, Jr., RN

Sponsor : CCNAPI Workshop 6 : (BMI Computation)” Main Preceptor : Beda B. Galicia, RN

Preceptors : Charliemagne M. Marinas, RN Raizzah T. Mansoura, RN John Christian M. Agustin, RN

Speaker : Cristy Rodondo, MD Sponsor : Abbott Nutrition Laboratories

5:00 pm – 5:30 pm CLOSING CEREMONIES Closing Remarks Convention Evaluation

Raffle Draw Distribution of Certificates

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PLENARY 1

“Rapid Response in Acute Brain Attack”

DAIWAI M. OLSON, PhD, RN, CCRN Associate Professor of Neurology & Neurotherapeutics Associate Professor of Neurosurgery, Staff Nurse, Neurocritical Care Unit

University of Texas Southwestern

Stroke is a leading cause of death and disability. While the signs and symptoms of

stroke range from subtle changes in verbal or cognitive ability to profound loss of

physical function, early recognition is vital to triaging patients for treatment. The

primary goal of early stroke treatment is aimed at reperfusion the cerebral cortex. New

pharmaceutical and mechanical strategies for reperfusion are now available worldwide

and have radically changed the chain of stroke survival. This session will discuss the

pathophysiology of stroke and early stroke treatment and management.

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Rapid Response in Acute Brain Attack

DaiWai M. Olson PhD RN CCRN Associate Professor of Neurology & Neurotherapeutics

Associate Professor of Neurosurgery University of Texas – Southwestern

Dallas, TX

Objectives: • Early recognition and identification of the signs and symptoms of stroke

• Triage and evaluate stroke patients • Strategies in preventing therapeutic delays • Updates in the Chain of Stroke Survival

• Approaches to early treatment and management

Acute Ischemic Stroke Versus Hemorrhagic Stroke

Stroke = disruption of blood flow to an area of the brain AIS = disrupts blood flow by clot ICH disrupts blood flow by diversion (secondary pressure)

SAH disrupts blood flow by diversion (secondary vasospasm) *Any Stroke = Brain Attack

Discussion: Primarily ischemic stroke

EARLY RECOGNITION AND IDENTIFICATION OF THE SIGNS AND SYMPTOMS OF

STROKE.

*To understand the signs and symptoms we need to have some understanding of the

pathophysiology.

Brain

• Brain does not store oxygen • Brain does not store glucose

• Apoptosis • Need to restore PERFUSION

How do we produce ENERGY?

Energy = ATP. ATP production is either aerobic or anaerobic.

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Energy Production

STEP 1: Glycolysis - Glycolysis produces 2 ATP. Without oxygen, pyruvate is converted into

lactate (lactic acid)

• Does not require oxygen

• Is the first step in converting food to energy

• Occurs in the cytoplasm

• Produces pyruvate and NADH

Kreb‟s(1937) Citric Acid Cycle

*You must have ATP and oxygen to initiate glycolysis .

Apoptosis - Cells are pre-programmed to commit SUICIDE. Neurons are „sort of‟ like lemmings

How can we disrupt apoptosis?

• Think about the pathway. It is more than just restoring blood FLOW.

Perfusion

-Perfusion is more than “blood flow”. The delivery of nutrient rich blood to biological tissues.

French “perfuser” = “to pour over”

Poisseulle‟s Theorem

Flow =(π) x (r2) x (perfusion pressure)/ (8) x (blood viscosity) x (vessel length)

*Flow is determined by the size of the pipe and pressure you are using to push it

through.Divided by. How thick the fluid is and how far it has to go.

Oxygen & Hemoglobin

- HgB has four polypeptide chains. Each chain has one heme group. Each heme group has one

iron ion. Each iron ion can bind with one O2 molecule. THEREFORE – each HgB can bind with 4

O2 molecules

Early recognition and identification of the signs and symptoms of stroke.

• FAST - Face, Arms, Speech and Time

• NIHSS - more complicated but more thorough. These are TOOLS, Primarily for

Healthcare Workers. There is, however, a good rule of thumb

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• MINOR STROKE / TIA

Triage and evaluate “ALL” stroke patients

Conclusions: Patients with TIA have

similar or worse

12-month post discharge risk of death or re-

hospitalization as compared with those with AIS.

Outcomes after TIA and AIS might be improved with

better adherence to secondary preventive guidelines.

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Preventing Delays

1. Communication & Teamwork

2. Process 3. Organizational Culture

4. Performance Monitoring & Feedback 5. Overcoming Barriers

What do we already know ?

• Early tPA improves outcomes in acute ischemic

stroke

• EMS pre-notification is not a standard of care

• EMS pre-notification might be helpful – but

data is limited

*Disclosures*

Dr. Olson is a member of the Duke Clinical Research Institute (DCRI) at Duke University. The

DCRI serves as the data coordinating center for the American Heart Association‟ Get With The

Guidelines programs.

Funding / Support: The Get With The Guidelines-Stroke (GWTG-Stroke) program is provided by

the American Heart Association/American Stroke Association. The GWTG-Stroke program is

currently supported in part by a charitable contribution from Bristol-Myers Squib/Sanofi

Pharmaceutical Partnership and the American Heart Association Pharmaceutical Roundtable.

GWTG-Stroke has been funded in the past through support from Boeringher-Ingelheim and

Merck.

*Evidence*

• Lin C, Peterson ED, Smith EE, Saver JL, Liang L, Xian Y, Olson DM, Shah BR,

Hernandez AF, Schwamm LH, Fonarow G. (2012).

Patterns, predictors, variations and temporal trends in emergency medical service

hospital pre-notification for acute ischemic stroke.

Journal of the American Heart Association.

DOI: 10.1611/JAHA.112002345.

• Lin C, Peterson ED, Smith EE, Saver JL, Liang L, Xian Y, Olson DM, Shah BR,

Hernandez AF, Schwamm LH, Fonarow GC. (2012)

Emergency medical service hospital pre-notification is associated with improved

evaluation and treatment of acute ischemic stroke.

Circulation: Cardiovascular Quality and Outcomes.

DOI:10.1161/CIRCOUTCOMES.112.965210

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Goal of this Study

1. Evaluate whether EMS pre-notification is associated with use of tPA among patients

arriving within either 3 hours or 4.5 hours

2. Evaluate if EMS pre-notification is associated with timeliness in acute ischemic stroke

evaluation and treatment, among those treated

Study Population

• Get With the Guidelines- Stroke

registry

• April 1, 2003 and April 2, 2011

• Final study population: 371,988

EMS-transported patients from 1,585

participating sites

Statistical Considerations

• Variable:

EMS pre-notification vs No EMS pre-

notification

• Outcomes

• Door-to-Imaging (DTI) time, DTI ≤

25min

• Door-to-Needle (DTN) time, DTN ≤

60min

• Arrival by 2h, treat by 3h

Univariate analysis: Pearson Chi-square test and Wilcoxon rank-sum test

Multivariable logistic regression analysis generalized estimating equations (GEE)

p = Probability

- Despite how improbable you may think an event is ... It may still happen!

“Chaz The Magnificent”

I was in Vegas and got to talking with the great and powerful (but homeless)

Chaz The Magnificent

Chaz wanted me to take him into the casino (he wasn‟t allowed in unless accompanied by someone who had bathed) and we would bet on roulette. C.t.M. guaranteed me that voices in his head could predict the outcome of any binomial distribution. And therefore – he wanted to play roulette…betting on red and black. I told C.t.M. that if he could demonstrate the ability to predict a random binomial event sufficiently such that he was better than chance… I would take him gambling (but only after he took a bath).

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I opted to test C.t.M. outside the casino – using the toss of a coin.

I toss a coin (not actually random…but close enough for our example)

If C.t.M. guesses (the voices tell him) correctly - - -Then the answer is “yes”

So, What can we say about C.t.M.

after 2 tosses of the coin?

Chance – and chance alone –

Gives a 0.25 probability that the voices in

C.t.M.‟s head will be correct

on 2 tosses of the coin.

I‟m not willing to gamble - YET

What would convince you?

How many times would C.t.M. have correctly state the coin toss before you

bet YOUR LIFE SAVINGS at roulette

based on the voices in his head?

Show of hands (2,3,4,5,6,7,8,9,10,20,50, 95)

There are 32 possible outcomes for the voices.

Only 1 of the 32 is Y-Y-Y-Y-Y

P(YYYYY) = 1/sum of all probable outcomes =

1/32 = .0250 = .03

Therefore “the voices are right (p < .05)”

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Differences in Treatment in Patients With EMS Pre-Notification vs Patients Without

*Pre-notification by Emergency Medical Services is Associated with More Timely Evaluation and

Treatment of Acute Ischemic Stroke.

Updates in the Chain of Stroke Survival

• The window for tPA is now 4.5 hours

• tPA is safe in the setting of Warfarin (INR <1.8) • TIA is just as bad – or worse – than AIS at 1 year

• Prenotification improves treatment time

Approaches to early treatment and management

• Thrombolytic – Medication (rt-PA Intravenous Or Intra-arterial?)

Approaches to early treatment and management

• Thrombolytic – Mechanical restoration of flow

• Penumbra / Merci / Etc

CAUTION!!

MR Rescue (results released 2/12/13)

Mechanical thrombectomy does not produce statistically significantly different results compared to conventional therapy.

Approaches to early treatment and management

• Perfusion

• (remember apoptosis) • Adequacy of oxygenation & blood flow • Blood Pressure management NO EVIDENCE

• Early Rehab (in the ICU)

• Restraint Therapy = No more “your arm doesn‟t work… learn to dress left handed”

• Neuroplasticity. “When do you stop learning?”

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Secondary Prevention

AVAIL: Hospital Recruitment

• AHA – GWTG hospitals (January 2006) – Roughly 300 hospitals

• Contacted to participate based on enrollment in GWTG-Stroke

– Actively enrolling

– Committed to continued enrollment

– Research coordinator/Site

coordinator

AVAIL: 12 month persistence by medication class

Patient-Related Factors and Persistence

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Approaches to early treatment and management

Transitions of Care

Olson DM, Prvu Bettger J, Alexander KP, Kendrick AS, Irvine JR, Wing L, Coeytaux RR, Dolor RJ, Duncan PW, Graffagnino C.

Evidence Report No. 202. (Prepared by the Duke Evidence-based Practice Center under

Contract No. 290-2007-10066-I.) AHRQ Publication No. 11(12)-E011. Rockville, MD. Agency for Healthcare Research and Quality.

October 2011. How was this done?

• 5,783 citations identified past 2000-2011

• 4605 – excluded based on title/abstract • 22 – excluded based on not original data

• 750 articles subjected for FULL READ • 668 – excluded (534-not transition, not peer, no data, no comparator, not stroke/MI) • 34 studies of 4,146* stroke patients

• 19 studies of 15,216 MI pts *Everything we know is based on less than 5,000 patients

Intervention – TYPE

1. Hospital-Initiated Support 2. Patient and Family education

1. hospital-based 2. home-based

3. Community-based Support

4. Chronic Disease management

*

In the interest of time = = = we will only look at

Hospital-Initiated Support

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Conclusion • Early Supported Discharge may be helpful

Certainly the most promising • For stroke – no other intervention had sufficient evidence of benefit to be

recommended. *only 34 studies in the history of man in the entire world

*only 18 studies of stroke and ESD

Caregivers

• Most often Spouse/partner (in transition studies) • But can be anyone

Usual care

• Most studies used “usual care” as their comparator, but few studies actually tell us what

usual care really is.

What does this mean?

• Stroke care continues to evolve • Nursing care is an important component of stroke care • There is much more work to be done

• YOU can do an important study ! ! !

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PLENARY II

“Interpretation of Dysrhythmias in ACLS”

MARIA ISABELITA C. ROGADO, RN, MAN Professor, Arellano University Graduate School of Nursing

In this age of the new millennium, EKG interpretation is an expected skill amongst

nurses not only in the critical care areas but in any setting where there is need for

cardiac monitoring. This skill in EKG interpretation is necessary particularly in the events

of resuscitation. It is essential that institutions have emergency policies and procedures

in place, along with a continuing competency education program and yearly refresher

programs. These programs should include validation of dysrhythmia interpretation skills

and problem solving of case studies.

This topic on Interpretation of Dysrhythmia in ACLS will tackle the basics of EKG

interpretation and how nurses can rapidly determine what they see on a scope or

rhythm so that appropriate and early management can be instituted. It will cover

dysrhythmias such as tachycardia and bradycardia in pre-arrest scenarios; shockable

and non-shockable rhythms during arrest scenarios and appreciation of ST elevation

during Acute Coronary Syndrome.

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INTERPRETATION OF DYSRHYTHMIAS IN ACLS

MARIA ISABELITA C. ROGADO, RN, MAN Professor,

Arellano University Graduate School of Nursing

OBJECTIVES

• Relate skills of dysrhythmia interpretation to clinical assessment and selection of

appropriate dysrhythmia treatment algorithm

• Discuss how dysrhythmia interpretation, patient assessment findings, and treatment

options are evaluated and selected

INTRODUCTION: THE BASICS

Newton‟s Third Law:

“To every action, there is equal and opposite reaction”

Cardiac Output: the amount of blood ejected by the left

ventricle in one minute

• Adult: 5-8 liters of ejected blood per minute.

• With strenuous activity, CO can increase to an amazing 25 liters per minute

• Cardiac Output = Stroke Volume x Heart Rate • Stroke volume is the amount of blood ejected by

the left ventricle with each contraction.

• SV = EDV - ESV

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CONDUCTION SYSTEM

Functions: 1. Generate electrical impulses

2. Conduct impulses to the heart muscles PQRST

P: Atrial depolarization

QRS: Ventricular depolarization

T: Ventricular Repolarization

PR: Conduction of the impulse from

SA node to the AV node

ST : End of Ventricular depolarization

and start of ventricular repolarization

INTRODUCTION: DYSRRHYTMIAS

• Clinical dysrhythmia interpretation must be made in conjunction with patient

assessment.

• Consider the effect that a particular dysrhythmia on a patient‟s well-being

• Determine the significance of the abnormal rhythm disturbance

• Decision can be made as to which therapy is indicated.

Case #1:

“The weak and dizzy elderly woman”

In the ED, a 64-year-old wife was complaining of dizziness and generalized weakness for the

last two hours.

The patient, awake and appearing weak, describes she had brief “passing out” while getting up

from the bed to go to the bathroom. She was feeling fine until about two hours ago, when she

suddenly became dizzy and had to be helped to lie down

The patient denies chest pain, shortness of breath, diarrhea, palpitations, nausea or vomiting,

blood in her bowel movements, abnormally dark stools, or prior episodes similar to today‟s

events.

Her past medical history is significant for hypertension for which she is taking a diuretic and an

ACE-inhibitor.

Her medication has not been changed recently, and she takes her medication as directed.

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Physical Examination:

• Alert and oriented;

• BP: 84/60 mmHg; PR: 36/min.; RR: 26/min.

• SpO2: 98% saturation.

• Her skin is pale and sweaty,

• Neck veins are not distended.

• Breath sounds: clear

• Heart sounds: regular without a murmur.

• Abdominal and neurologic examinations are normal

Initial Action:

• Oxygen is administered and

• Monitoring (cardiac) is started along with

• Insertion of an intravenous intermittent infusion device.

The ECG monitor recorded the tracing

*Third Degree Heart Block

with ventricular beat at 37

bpm

• Independent atrial (P) and ventricular (QRS) activity

• Very slow regular ventricular rhythm

• QRS complexes are wide and distorted, (low ventricular escape pacemaker)

• P-R intervals have no constant value; unrelated; being paced differently

BRADYCARDIA ALGORITHM

• Symptomatic bradycardia: a heart rate less than 60 bpm that elicits signs and symptoms

• Symptomatic bradycardia exists when the following 3 criteria are present:

1.) The heart rate is slow;

2.) The patient has symptoms; and

3.) The symptoms are due to the slow heart rate

*Functional or relative bradycardia occurs when a patient may have a heart rate within normal sinus

range, but the heart rate is insufficient for the patients condition. An example would be a patient with an

heart rate of 80 bpm when they are experiencing septic shock.

Decrease Cardiac Output

• Signs: – Hypotension

– Orthostatic HpN

– Diaphoresis

– Pulmonary congestion on PE and CXR

– Congestive Heart Failure

– Pulmonary Edema

– Brady-related frequent escape PVC or

VT

• Symptoms: – Chest discomfort or pain

– Shortness of breath

– Decreased level of

consciousness

– Weakness

– Fatigue

– Light headedness

– Dizziness, syncope

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Unstable Persistent Bradycardia

• Atropine

– First Dose: 0.5 mgs bolus

– Repeat every 3-5 minutes

– Maximum: 3 mgs

• Transcutaneous Pacing

• Dopamine Infusion

– 2-10 mcg/kg per minute

• Epinephrine Infusion

– 2- 10 mcg/minute

Sinus Bradycardia

Rhythm : Regular

Rate : less than 60 BPM P waves : present before every QRS consistent in shape

PR interval : usually normal QRS : usually normal Conduction : normal

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FIRST DEGREE AV BLOCK

Rate : Usually within normal range, but depends on the underlying

rhythm

Rhythm : Regular

P waves : Normal in size and shape

PR interval : prolonged (>0.20 sec) but constant

QRS duration : Usually 0.10 sec or less unless an intraventrucular conduction

delay exists

FIRST DEGREE AV BLOCK

• Not a dysrhythmia itself

• Condition describing the consistent prolonged PR interval

• Impulse from SA to ventricles are delayed (not blocked) in the AV node

What Causes it?

• Ischemia

• Medications

• Rheumatic Heart Disease

• Hyperkalemia

• Acute MI (Inferior wall MI)

• Increase vagal tone

FIRST DEGREE AV BLOCK

What Do I Do About It?

• First Degree AV Block in acute MI must be monitored closely

• Symptomatic bradycardia – Treat bradycardia!

• Oxygen

• IV access

• IV Atropine

• Transcutaneous pacing

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SECOND DEGREE AV BLOCK

Type I (Wenckebach, Mobitz Type I)

Rate : Atrial rate is greater than ventricular rate Rhythm : Atrial Regular, ventricular irregular

P waves : Normal in size and shape, some Pws are not followed by QRS PR interval : Lengthens with each cycle

QRS duration : Usually 0.10 sec or less but is periodically dropped

• Wenckebach pattern is the progressive lengthening of the PR interval followed by a P

wave with no QRS

• Conduction delay happens at the level of the AV node

What Causes it?

• Associated with RCA block (supplies AV node in 90% of the population)

• Disturbance in the balance between sympathetic and parasympathetic divisions

• Increase in parasympathetic tone – conduction in AV is slowed down

What Do I Do About It?

• Symptomatic due to meds – Stop medication!

• Slow heart rate with serious symptoms

• Atropine

• Temporary Pacing

• Observe closely for increasing AV block

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Type II (Mobitz Type II)

Rate : Atrial rate is greater than ventricular rate, VR often slow

Rhythm : Atrial Regular, ventricular irregular

P waves : Normal in size and shape, some Pws are not followed by QRS

PR interval : Within normal limits or slightly prolonged but constant for the

conducted beats. There may be some shortening of the PRI that follows a nonconducted beat

QRS duration: Usually 0.10 sec or greater, periodically absent after Pw

• Conduction delay occurs below the AV node (Bundle of His or at the level of the Bundle

Branches

• More serious than Mobitz I

• Often progresses to complete heart block

What Cause It?

• LCA supplies the bundle branches

• Acute myocarditis

• Anterior MI

• Other types of organic disease

2:1 Conduction (2:1 AV Block)

• Two pw occur for every QRS (2:1 conduction)

• Narrowed QRS - associated with Second Degree Type 1

• Wide QRS – associated with delay in the conduction below the AV node and is usually a

type II block

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What Do I Do About It?

• Prepare for pacing

• Atropine should be avoided

• Will not improve the block but will increase the rate of discharge of the SA node

• Triggers the situation in which fewer impulses are conducted through the

ventricles therefore VR is furthered slowed down

THIRD DEGREE AV BLOCK

COMPLETE HEART BLOCK

Rate : Atrial rate is greater than the ventricular rate, VR is determined by origin

of the escape rhythm

Rhythm : Atrial Regular, ventricular Regular

P waves: Normal in size and shape

PR interval : None

QRS duration : Narrow or wide depending on the location of the escape pacemaker and

the condition of the intraventricular conduction system.

(Junctional = narrow; Ventricle= wide)

SA impulse are blocked before reaching the ventricles so no Pw are conducted Atria and ventricle beat independently from each other AV block may occur in AV node, BH or BB

A secondary pacemaker, either juctionnal or ventricular, stimulates the ventricles QRS may be narrowed or wide, depending on the location of the escape pacemaker and a condition of intraventricular conduction system

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What Caused it? • Associated with an inferior MI

• Result of a block above the Bundle of His • Resulting rhythm is usually stable

• Escape pacemaker is usually junctional (narrow QRS) • VR of more than 40 bpm

What Do I Do About It? • Narrow QRS and symptomatic due to slow rate • Wide QRS and symptomatic

• Transcutaneous Pacemaker (TCP)

Bradycardia Algorithm 2010 AHA Update: For symptomatic bradycardia or unstable bradycardia IV infusion chronotropic agents (dopamine & epinephrine) is now recommended as an equally effective alternative to external pacing when atropine is ineffective.

Case #1 Treatment Considerations

• A : alert; good airway • B : adequate breathing, clear breath sounds; RR=26 SpO2 = 98%

• C : inadequate; slow HR (37 bpm), but not in need of cardiac compressions; BP = 80/60; signs of adrenergic discharge: pallor and diaphoresis

• D: dizzy with loss of consciousness initially; Now: alert and oriented; neuro check is

normal patient‟s symptoms appear to be directly related to her slow heart rate.

Causes

• Third-degree heart block in elderly patients is usually due to gradual fibrosis of the A-V conduction system

• The patient needs to be assessed and treated as if she were experiencing an acute coronary event

Treatment Plan

• Emergency Cardiac Care Treatment Algorithm for Adult Bradycardia • Stable or Unstable (?)

• Start with either atropine or artificial pacing

Case #2:

“The case of the man who „passed out‟ during his dialysis session.” • A 70-year-old male with a history of hypertension, end stage renal disease, and insulin-

dependent diabetes mellitus arrives in the emergency department

• He experiencing a brief syncopal episode during his dialysis treatment thirty minutes before arrival.

• The patient diaphoretic and hypotensive and was administered oxygen and 500 cc of normal saline in the Dialysis Center.

• This occurred just as he was finishing his dialysis session.

• His bedside glucometer determination was 140 mg/dl.

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• Vital signs in the ED: • BP: 130/60 mmHg

• PR: regular at 150/min. • RR: 26 bpm

• The patient is alert, and afebrile • His lung sounds are clear and there is no pedal edema. • He denies chest pain or shortness of breath but is complaining of palpitations, nausea,

and generalized weakness.

*Atrial flutter with a 2:1 A-V conduction and a rapid ventricular rate at 150/minute

• The rhythm is grossly regular with a rapid ventricular rate, • ventricular (QRS) complexes are narrow. • P waves are not visible; seen as flutter waves,

• The ST segments are difficult to evaluate due to the flutter waves. • The A-V relationship consists of 2:1 conduction,

• Ventricular rate of 150/minute is very fast for a patient with limited cardiac reserve. TACHYDYSRHYTHMIAS

• Narrow-QRS Tachycardias • Wide-QRS Tachycardias • Irregular Tachycardias

• Atrial Flutter • Atrial Fibrillation

• Supraventricular Tachycardia (SVT) • Monomorphic VT • Polymorphic VT

• Wide-complex tachycardia of uncertain type

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Sinus Tachycardia

Rhythm : Regular

Rate : faster than 100 BPM P waves : present before every QRS

consistent in shape may be hidden in Tw PR interval : normal, difficulty to measure

QRS : usually normal Conduction : normal

Atrial Flutter

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Atrial Fibrillation

Supraventricular Tachycardia (SVT)

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Tachycardia Algorithm

• An unstable tachycardia exists when cardiac output is reduced to the point of causing

serious signs and symptoms. • Serious signs and symptoms commonly seen with unstable tachycardia are:

chest pain, signs of shock, HpN altered mental status,

weakness, fatigue, and syncope • The most common causes of tachycardia that should be treated outside of the ACLS

tachycardia algorithm are:

dehydration, hypoxia,

fever, and sepsis Administration of OXYGEN and NORMAL SALINE are of primary importance for the treatment of

causative factors of sinus tachycardia and should be considered prior to ACLS intervention.

There may be other contributing causes and review of the H‟s and T‟s of ACLS should take

place as needed.

• Is the patient responsive?

• A-B-C-D – Oxygen (4L/m) – Hook the patient to

the monitor – Start an IV access

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• Stable (narrow QRS complex) → vagal maneuvers → adenosine 6 mgs (if regular)

→ beta-blocker/calcium channel blocker → get an expert

• Stable (wide/regular/monomorphic) → adenosine (regular and monomorphic) →

consider antiarrhythmic infusion (Procainamide 20- 50 mgs / min; Amiodarone 150 mgs)

→ get an expert

• Unstable tachycardia should be treated immediately with synchronized

cardioversion.

2010 ACLS GUIDELINES

Synchronized Cardioversion

Atrial Fibrillation • Biphasic – 120J • Monophasic – 200J

Atrial Flutter/SVT • Biphasic/Monophasic – 50-100J

Monomorphic VT • Biphasic/Monophasic – 100J

New Medication Protocols

• Adenosine is recommended in the initial diagnosis and treatment of stable,

undifferentiated regular, monomorphic wide-complex tachycardia

• It is important to note that adenosine should not be used for irregular wide-complex

tachycardias because it may cause degeneration of the rhythm to VF.

• Indication: • PSVT

IV Dose: 6 mg bolus followed by 12 mg in 1-2 minutes if needed *Adenosine IV Bolus

• Very short half-life • Rapid bolus • 6 mg given as a rapid intravenous bolus (administered over a 1-2 second period) • Followed by 20 cc NSS • Elevate arm / site

Case #3: “The case of the hospitalized patient recovering from an MI.”

• A 54-year-old man, was recovering in the • intensive care unit from an uncomplicated inferior wall MI that he experienced 24 hours

before. • Thrombolytic therapy opened the occluded coronary artery and his chest pain, along

with the acute ECG changes, subsided. • The nurse went to his room in response to a dysrhythmia alarm and found the patient

unresponsive, propped up in bed, not breathing, and without a pulse.

• The nurse summoned help, lowered the head of the bed, and observed the ECG rhythm

30

The ECG monitor recorded the tracing

• The rhythm consists of a rapid, disorganized ventricular tachydysrhythmia.

• Distinct QRS complexes are absent. • The ECG baseline zigzags across the tracing. • Discrete P waves are also not visible, AV relationship cannot be determined.

• The patient‟s clinical appearance confirms the interpretation

Initial Treatment Considerations

• Goal: to convert this life-threatening ECG dysrhythmia to a nonlethal rhythm.

• Initiate countershock as rapidly as possible at 360 joules

• Start CPR

• Epinephrine and Amiodarone

SHOCKABLE RHYTHMS

• Pulseless Ventricular Tachycardia (PVT)

• Ventricular Fibrillation

Pulseless VT / VF Algorithm

• Ventricular Tachycardia

– Monomorphic

– Polymorphic

– Torsades de Pointes

• Ventricular Fibrillation

– Course

– Fine

31

32

33

*Fine VF

*Course VF *The best hope for resuscitation remains early detection and early defibrillation. For persistent or recurrent ventricular fibrillation or pulseless ventricular tachycardia, consider the following anti-arrhythmic therapies: Amiodarone in a 300-mg rapid intravenous bolus. Lidocaine (1 mg/kg) intravenously. Magnesium sulfate in a 1- to 2-g dose for polymorphic forms of VT or in known

hypomagnesemic states. Procainamide IV at 30 mg/min up to 17 mg/kg (average of 1200 mg per 70-kg

patient) can be given for refractory cases, but it is not recommended because it is often not practical to administer during cardiac arrest due to the preparation and administration time

Non-Shockable Rhythms

• Pulseless Electrical Activity (PEA)

• Asystole

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Case #4: “The case of a pulseless rhythm”

• The nurse went to his room in response to a dysrhythmia alarm and found the patient unresponsive, propped up in bed, not breathing,

and without a pulse. • The nurse summoned help, lowered the head of the bed, and

observed the ECG rhythm

Pulseless Electrical Activity

• Always check the pulse with the rhythm

• Vassopressor (IV / IO) – Epinephrine 1 mg repeat every 3-5 minutes – Vassopressin 40 units

• Administer drugs during CPR. Do not stop CPR to administer drugs. • Consider advanced airway and capnography

Asystole

• Things to check to ensure that this is true asystole: – loose leads or leads not connected to the patient;

– signal gain; – ensure that the patient is pulseless – You confirm that this is true asystole and that the patient has no pulse. You begin the

pulseless arrest algorithm. Your first step is to: – Begin CPR immediately – Give epinephrine 1 mg IV/IO

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2010 ACLS Guidelines *New Medication Protocols

• Atropine is not recommended for routine use in the management of PEA/asystole and

has been removed from the ACLS Cardiac Arrest Algorithm

• Indications: • Symptomatic sinus bradycardia

• Second Degree Heart Block Mobitz I • IV Dose:

• .5 – 1 mg every 3-5 minutes • Max dose is .04mg/kg • Can be given down ET tube?

36

PLENARY III

“Challenges in Sepsis Management”

DAIWAI M. OLSON, PhD, RN, CCRN Associate Professor of Neurology & Neurotherapeutics

Associate Professor of Neurosurgery, Staff Nurse, Neurocritical Care Unit University of Texas Southwestern

Every critical care nurse is challenged to provide care to patients with sepsis and prevent sepsis

in patients at risk. The evidence-based practice for sepsis prevention is evolving from a robust

debate. Key to this discussion is an understanding of the pathophysiology of sepsis, including

identifying at risk populations. This session is aimed at discussing evidence for the role of the

nurse in both prevention and treatment of sepsis in the ICU setting.

37

“Challenges in Sepsis Management”

DAIWAI M. OLSON, PhD, RN, CCRN Associate Professor of Neurology & Neurotherapeutics

Associate Professor of Neurosurgery, Staff Nurse, Neurocritical Care Unit

University of Texas Southwestern

OBJECTIVES • Present factors that increase the risk of developing or preventing sepsis

• Discuss strategies / methods of prevention and early detection of Sepsis

• Discuss the current trends and advances in caring and managing sepsis

• Roles of the nurse in the prevention and management of sepsis

PATHOPHYSIOLOGY

In order to understand the body's response to sepsis, we must first review the pathophysiology.

Sepsis is a complex process; it is the body's systemic response to an infection. When the body

is unable to contain a localized infection at its source, the infecting organism leaks into the

bloodstream, causing sepsis. This is associated with inflammation, coagulopathy, and the

maldistribution of blood flow.

When the invading organism, or antigen, enters the bloodstream, it releases endotoxin, a toxic

substance usually associated with gram-negative bacteria. In response, the body's immune

system releases proinflammatory mediators, such as prostaglandins and cytokines, including

tumor necrosis factor and interleukins, into circulation.2,3,5 Cytokines are immunomodulators

released by white blood cells in response to the endotoxins, and together they are responsible

for causing vasodilatation, increased capillary permeability, and increased coagulation.5,6 In a

healthy person under normal circumstances, the body can control these processes and heal; but

in the septic patient, the endotoxins stimulate the release of too much of the

immunomodulators, causing an exaggerated, excessive response.3

Vasodilatation is the body's way of increasing blood flow to the affected area, thereby

transporting more white blood cells, such as macrophages, to control the original infection.

However, vasodilatation, without a proportionate increase in blood volume, leads to

hypotension. Increased capillary permeability allows fluid to leak out of the blood stream and

into surrounding tissue, causing edema. This further reduces blood pressure. Concurrently,

fibrinolysis is impaired leading to a decrease in clot breakdown. This is thought to be the body's

38

attempt at confining the antigen.3 However, the formation of fibrin clots leads to microthrombi,

causing hypoperfusion of tissues, tissue necrosis, and eventually organ failure.

SEPSIS IS NOT.. • Just a bad infection • An infection that has spread

• Systemic infection • Infection in the bloodstream (Septicemia)

• A viral infection • Determined by length of stay

Sepsis is a response to infection in which there is an interruption in the tissue perfusion to

vital organs

Heart Attack = interrupted perfusion to myocardium (caused by clot or plaque)

Brain Attack = interrupted perfusion to cerebral cortex (caused by clot or hemorrhage) Sepsis = interrupted perfusion to multiple vital organs (caused by infection)

Sepsis is an Emergency. ~ 35% of patients with sepsis will die. Early recognition and treatment is associated with higher recovery rate. Without treatment Sepsis will usually

progress to Septic Shock. ~50-75% of patients with Septic Shock will die.

Odds Ratio • Odds ratios are most typically used for case-control studies. • Odds ratios estimate the relative risk of a rare event being observed in some population

Possible versus Probable It is POSSIBLE that I will be attacked by a shark …. But . . . Is it PROBABLE that I will be

attacked?

For Humans

Likelihood of shark attack is 17/100,000,000 = 0.00000017 Likelihood of attack for swimmers is 16/44,787,203 = .000000036

Odds of shark attack for swimmers vs non-swimmers is X2 = 19.724

39

RISK of SHARK ATTACK among

• Did you go swimming at

DUSK?

• Did you get attacked by a

shark?

SO - - how do we interpret ?

Answer -- -- don‟t swim at DUSK

DUSK increases RISK.11 – thousand

times more likely If you swim and

You swim at dusk

For SWIMMERS

Likelihood of a shark attack is 15/44,787,203 = 0.00000349

Likelihood of shark attack for dusk swimmers is 15/59,795 = 000251

Odds of shark attack swimming dusk vs daytime = X2 = 11237.13

40

Factors that increase the risk of developing sepsis

• Very young - Very old • Very poor - Very rich

• Already sick – Infirm

• Post surgical / at home

– Hospitalized – Drug / Alcohol

– Cancer • Chemotherapy

• Open wounds/injuries (including trauma)

• Treatment conditions – Foley catheter – IV catheters

• Central Line – Wound drainage collection

– Immobility – Antibiotic – Hx Resistant infection (MRSA, VRE)

Dengue Fever / Dengue virus

• Dengue Fever does not CAUSE sepsis! …..BUT…. Dengue Fever may result in weak,

infirm, body in which a bacterial infection may result in sepsis.

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Preventing sepsisfor patients WITH infection present

• Prompt recognition of the initial infection

– NURSING CARE = INSPECT !

• Good Health

• Good Nutrition

• Prevent spread of the infection

– Between organ systems

– To new tissue(s)

• Prevent new infection

– Secondary organism

Early Recognition

• Signs & Symptoms of infection

– Rubor = redness

– Tumor = swelling

– Dolar = pain

– Calor = heat

– Loss of Function

Prevention Strategies

• Bundles

– VAP, ICU, Central Line

• Handwashing campaigns

• SCIP (Surg Care Imp Prog)

• CHECKLIST MANIFESTO

• 10,000 lives campaign

• Environmental controls

– Healthier Hospitals Initiative

Specific Examples

• Pre-op check (“is this the right patient?”)

• LeapFrog

• VAP Bundle

• 100,000 lives

• Healthier Hospitals Initiative

• Closing the Gap Initiative

*Not a single initiative has resulted in more harm than good!

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The Checklist Manifesto

Atul Gawanda

Perhaps the „best known‟ medical safety initiative

“Despite your ownpersonal awesomeness,

a checklist can help you.”

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IHI

Institute for Healthcare Improvement

• IHI MRSA infection prevention – Screening – Preventive cross contamination

– HANDWASHING !

When does an Infection become SEPSIS?

• Disruption of perfusion to more than one organ/system

– Don‟t forget the SKIN

– Bladder

– Blood stream

– CSF

– Gut (multiple organs)

– Lymph

– Lungs

Systemic Inflammatory Response Syndrome (SIRS)

“OFTEN” preceeds SEPSIS

TWO or MORE of the below = SIRS

• Body temperature < 36C or > 38C

• Heart rate greater than 90 /min

• Hyperventilation (respiratory rate > 20 /min)

• PaCO2 < 32 mm Hg (normal 35 to 45 mm Hg)

• WBC > 12,000/mm3 or <4,000/mm3 (normal 5,000 to 10,000/mm3)

In addition to rubor, tumor, dolar, calor, loss of function

– Altered mental status

– Acute oliguria (urine output <0.5 ml/kg/h)

– Hyperglycemia in the absence of diabetes

– Hypoxemia

– Coagulopathy (INR > 1.5)

– Gastric ileus

Current trends and advances in caring and managing sepsis

- www.survivingsepsis.org

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PRESSURE. A comparison of size and volume

PERFUSION. The delivery of nutrient rich blood to biological tissues

FLOW.

Poiseuilles‟ Theorem – This Address the flow.

Radius becomes the most

important determinant of CBF

Length is often considered a constant

Viscosity (think Hct)

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How can you measure BP? McKay D.W.

Measuring blood pressure: a call to bare arms? Canadian Med Assn Journal. Feb 26 2008;178(5):591-593.

Key points of the article

• B/P readings are indirect measurements - accuracy depends on factors related to the patient

and the equipment.

• Automated cuffs, despite having clinical approval, may be inaccurate in some individuals for

reasons that are not well understood.

• Advances in the technology warrant a re-examination of the assumptions underlying B/P

measurement.

• Differences in patients and product may limit the generalizability.

Where can you measure BP?

Auscultation

• Arm

• Wrist

• Finger

• Thigh

• Ankle

Intra-arterial

• Radial

• Brachial

• Femoral

• Pedal

• Jugular

• Aorta

How can you measure perfusion?

• Mean arterial pressure (MAP)

• Oxygen extraction (O2ER)

• Measures of blood flow

– Velocity

– Stroke volume

• Measures of Metabolism

Why „did‟ we think MAP was a reflection of perfusion?

MAP = DBP + 1/3 SBP

MPAP = PDias + 1/3 PSys

Perfusion – Oxygenation

Supply side

• Arterial blood gas • Oxygen availability

(CaO2)

• Oxygen delivery

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Arterial blood gas

• pH

• PaCO2

• Bicarb

• PaO2

Oxygen availability (CaO2)

– Hemoglobin

• 1.38 = the milliliters of oxygen carried per gram of hemoglobin (1.34 –

1.39)

– Dissolved oxygen / PaO2

– Arterial oxygen content

• Formula

– CaO2 = arterial oxygen content

– CaO2 = Hgb x SaO2 x 1.38 + (0.0031 x PaO2)

• Normal values

– CaO2 = 17 – 20 ml O2 / 100 ml blood

Oxygen delivery (DO2)

– Hemoglobin

• 1.38

– Cardiac output

• Stroke volume x Heart rate

– Formula

• DO2 = oxygen delivery

• DO2 = CO x Hgb x SaO2 x 1.38 x 10

– Normal values

• DO2 = 900-100 ml/min

• DO2I = 360-600 ml/min/m2

Demand Side

Venous oxygen content (CvO2)

– SvO2

• SvO2 = DO2 – VO2

• Normals= 60 – 75 mmHg

– Venous oxygen content

• Formula

– CvO2 = venous oxygen content

– CvO2 = Hgb x SvO2 x 1.38 + (0.0031 x PvO2)

• Normal values

– CvO2 = 13 – 16 ml O2 / 100 ml blood

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Oxygen consumption (VO2)

– Formula

• VO2 = oxygen consumption

• VO2 = (CaO2 –CvO2) x CO x 10

• VO2 = CO x Hgb x (SaO2 –SvO2) x 1.38 x 10

– Normal values

• VO2 = 220-290 ml/min

• VO2I = 108-165 ml/min/m2

Oxygen balance

Oxygen extraction ratio (O2ER)

• Formula

– O2ER = oxygen extraction ratio

– O2ER = [ ( CaO2 –CvO2 ) / CaO2 ] x 100

• Normal values

– O2ER = 22% - 30%

– O2ERI = 20% - 25%

Where can you measure perfusion?

• Local –

– at the tissue/organ level. Licox and Thenar eminence

• Referred –

– measures of systemic perfusion. *Caution: Maybe – but is this referred? What is inferred?

• Inferred –

– Oxygen delivery

– blood pressure

How can you measure flow?

• Direct –

– Invasive

– NIRS

– Doppler

• Indirect

– PICCO – LiDCO – Flotrac - Cheetah

Transcranial Doppler

• assesses intra-arterial velocities of blood flow through the cerebral arteries.

• Increase in velocity = vasospasm

• Operator dependent.

Roles of the nurse in the prevention and management of sepsis

-Aseptic Technique

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Urosepsis

• Sterile insertion ! ! !

• Clean catheter and meatus

• Drain often

– Not the same as EMPTY often

• Remove early

Up and GO

• This is a great opportunity for nursing research

• Make the patient get up and GO

– Early foley catheter removal

Decubiti as source

• Mobility / Turning

H.A.P.

• Bundle

• Oral care

• Subglottal suction

• NO SALINE LAVAGE

• Elevate HOB

Roles of the nurse in the prevention and management of sepsis

• Front Lines

– Prevent initial infection

– Recognize any infection

– Prevent spread of infection

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PLENARY IV

“Nuts and Bolts in Neonatal Resuscitation”

WILFREDO R. SANTOS, MD, FPPS, FPSNBMJ

President,

Philippine Society of Newborn Medicine

This lecture is about the indications of neonatal resuscitation, its risk factors. It will also discuss

updates on resuscitation based on the 16th edition of Neonatal Resuscitation Program (NAP) of

the AHA and AAP.

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NUTS & BOLTS IN NEWBORN RESUSCITATION

Why the NEED to LEARN Neonatal Resuscitation?

• Approximately 10% of newborns require some assistance to begin breathing at birth • Less than 1% require extensive resuscitative measures

Risk Factors Associated with the Need for Neonatal Resuscitation

• ANTEPARTUM FACTORS Maternal DM Post-term gestation

Pregnancy-induced HPN Multiple gestation

Fetal anemia / isoimmunization Size-dates discrepancy

Previous fetal or neonatal death Drug therapy such as Magnesium

Bleeding in 2nd or 3rd trimester sulfate, adrenergic-blocking drugs

Maternal infection Maternal substance abuse

Maternal cardiac, renal, pulmonary, Fetal malformation or anomalies

thyroid or neurologic disease Diminished fetal activity

Oligo/polyhydramnios No prenatal care

PROM Maternal age< 16 or >35 years

Fetal hydrops

• INTRAPARTUM FACTORS

Emergency CS Persistent fetal bradycardia

Forceps or vacuum-assisted delivery Non-reassuring fetal heart rate patterns

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Breech or other abnormal presentation Use of general anesthesia

Premature labor Uterine hyperstimulation

Precipitous labor Narcotics administered to mother

Chorioamnionitis within 4 hours of delivery

PROM > 18 hours before delivery Meconium-stained amniotic fluid

Prolonged labor > 24 hours Prolapsed cord

Prolonged second stage of labor >2 hours Abruptio placenta

Macrosomia Placenta previa

Significant intrapartum bleeding

Clinical Manifestations which may need neonatal resuscitation

• Apnea • Bradycardia

• Cyanosis • Pallor • Congenital anomalies like diaphragmatic hernia, upper airway anomalies, neurologic

anomalies • Prematurity : at higher risk of resuscitation

Why are premature babies at higher risk of resuscitation?

• Surfactant deficiency • Immature brain development • Weak respiratory muscles

• Rapid heat loss which may be due to thin skin, large body surface area, decreased fat • Susceptible to hypovolemic shock due to small blood volume • Immature immune system

Rapid Assessment of the 3 Characteristics

• Term gestation? • Crying or breathing? • Good muscle tone?

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• If the answer to all 3 of these questions is “YES” the baby does NOT need resuscitation and should not be separated from the mother (dried, skin-to-skin, initiate breastfeeding)

• Observe for Breathing, Activity and Color

• If the answer to ANY of the 3 Assessment Questions is “NO” the infant should receive one or more of the following 4 categories of action in sequence:

A. Initial Steps in stabilization (provide warmth, clear airway if necessary, dry, stimulate)

B. Ventilation

C. Chest compressions

D. Administration of epinephrine and/or volume expansion

How Do You Prepare for a Resuscitation

• At every birth, you should be prepared to resuscitate a newborn because the NEED for resuscitation can come as a complete SURPRISE!

• With careful consideration of risk factors, more than half of all newborns who will need resuscitation can be identified prior to birth.

• Recruit additional skilled personnel • Prepare the necessary equipment

Why is Apgar Score not used to guide resuscitation

• The Apgar Score is NOT used to determine the need for resuscitation, what resuscitation steps are necessary, or when to use them

Initial Steps of Stabilization

• Provide warmth • Position the baby : “sniffing position” • Clear the airway

• Dry the baby • Stimulate breathing

Provide Warmth

• Temperature control:

> prewarming the delivery room to 26‟C

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> covering the baby in plastic wrapping

> exothermic mattress

> under radiant heat source

> swaddling

> skin-to-skin

> prewarming the linen

Clearing the airway

• When amniotic fluid is clear:

• It is recommended that suctioning immediately following birth should be reserved for

babies who have obvious obstruction to spontaneous breathing or require PPV

• When meconium is present:

• In the absence of RCT‟s there is insufficient evidence to recommend a change in the current practice of performing ET suctioning on non-vigorous babies with MSAF.

• If attempted intubation is prolonged and not successful, bag-mask ventilation should be considered, especially if with bradycardia

Assessment of Oxygen Need and Administration of Oxygen

• There is a large body of evidence that blood oxygen levels in umcompromised babies generally do not reach extrauterine values until approximately 10 minutes following birth

• The use of Pulse oximeter • Administration of supplementary oxygen

• PPV if heart rate < 100 bpm after the initial steps

Endotracheal Intubation

• Initial endotracheal suctioning of nonvigorous meconium-stained newborns • If bag-mask ventilation is prolonged or ineffective • When chest compressions are performed

• For special conditions like, congenital diaphragmatic hernia or ELBW and extremely premature babies

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Chest Compression

• Indicated for a heart rate that is < 60 per minute despite adequate ventilation with

supplementary oxygen for 30 seconds. • Thumb technique and the two finger technique

• 3:1 ratio of compressions to ventilations with 90 compressions and 30 breaths

Medications

• Epinephrine : preferred is IV route • Recommended dose is 0.01-0.03 mg/kg/dose • Volume expansion with crystalloid solution or blood at 10 ml/kg

• Naloxone is not recommended

Post-resuscitation Care

• Electrolytes and metabolic imbalance corrected

• Induced therapeutic hypothermia • Nutritional support: carbohydrates and protein on the first 24 HOL ( protein may be

given at 3 gm/kg)

• Antibiotics if warranted

Guidelines for Withholding and Discontinuing Resuscitation

• Extreme prematurity (AOG <23 weeks or BW<400 grams) • Anencephaly

• Trisomy 13 • In conditions associated with uncertain prognosis in which survival is borderline, the

morbidity rate is high, and the anticipated burden to the child is high, parental desires

concerning initiation of resuscitation should be supported

Discontinuing Resuscitative Efforts

• In a newly born with no detectable heart rate it is appropriate to consider stopping resuscitation if the heart rate remains undetectable for 10 minutes

The Evidence

• Extensive review of evidences for the guidelines on newborn resuscitation were

presented in the 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations

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• The above evidences are the basis for the 6th edition (2011) of the Neonatal Resuscitation Program of the AHA and AAP

NRP 2010: SCIENCE CHANGES

www.newbornwhocc.org/pdf/NRP2010-Changes.pdf

Resuscitation step

Recommendations (2005)

Recommendations (2010)

Comments/LOE

1) Assessment for need of resuscitation Four questions

Four questions 1. Gestation-term or

not? 2. Amniotic fluid-

clear or not? 3. Tone- Good? 4. Breathing /Crying?

Three questions 1. Gestation-

term or not? 2. Tone- Good? 3. Breathing

/Crying?

• Instead of 4 questions now 3 questions are asked at initiation of resuscitation. • “Amniotic fluid- clear or not” not part of assessment at birth. However, tracheal suction of non-vigorous babies with meconium stained amniotic fluid (MSAF) still to be continued (part of clearing airway in initial steps)

2005 2010 Remarks

2) Routine care (Given if answer to all three question is YES)

• Provide warmth • Clear airway • Dry • Assess color

• Provide warmth • Clear airway • Dry • Assess color

Emphasis on placing baby on mothers chest in skin to skin contact

3) Initial steps • Provide warmth • Position; Clear airway(if required) • Dry, stimulate, reposition

• Provide warmth • Open airway( no routine suction) • Dry , stimulate

• No change except for terminology

2) Routine care (Given if answer to all three question is YES)

• Provide warmth • Clear airway • Dry • Assess color

• Provide warmth • Clear airway • Dry • Assess color

Emphasis on placing baby on mothers chest in skin to skin contact

3) Initial steps • Provide warmth • Provide warmth • No change except

56

• Position; Clear airway(if required) • Dry, stimulate, reposition

• Open airway( no routine suction) • Dry , stimulate

for terminology

4) Assessment (after initial steps and ongoing) 4.1) Assessment for need for progressive steps after initial Steps 4.2) Assessment of heart rate

Look for 3 signs • Hear rate • Color • Respiration Palpation of umbilical cord pulsation for 6 sec and multiply by 10

Look for 2 signs • Heart rate • Respiration( Labored, unlabored, apnea, gasping) Auscultation of heart at the precordium is the most accurate

• Color has been removed from the signs of assessment • Pre-cordial auscultation better than umbilical cord palpation for detection of heart rate (LOE2, LOE4)

4) Assessment (after initial steps and ongoing) 4.1) Assessment for need for progressive steps after initial Steps 4.2) Assessment of heart rate

Look for 3 signs • Hear rate • Color • Respiration Palpation of umbilical cord pulsation for 6 sec and multiply by 10

Look for 2 signs • Heart rate • Respiration( Labored, unlabored, apnea, gasping) Auscultation of heart at the precordium is the most accurate

• Color has been removed from the signs of assessment • Pre-cordial auscultation better than umbilical cord palpation for detection of heart rate (LOE2, LOE4)

5) Positive pressure ventilation (PPV) 5.1) Indication for PPV 5.2) Assessment of effectiveness of resuscitation steps once PPV is started

Indications are(any 1 out of 3)

1. Hear rate < 100/min

2. Apnea or gasping

3. Persistent central cyanosis despite free flow oxygen

Heart rate Color Respiration

Indications (1 out of 2) 1. Hear rate

< 100/min

2. Apnea or gasping

Heart rate Pulse oximetry Respiration

• Persistent central cyanosis is not mentioned in the indication for PPV; use pulse oximetry to assess oxygenation • Increase in HR most sensitive indicator of resuscitation efficacy (LOE5)

5) Positive pressure ventilation (PPV) 5.1) Indication for PPV 5.2) Assessment of effectiveness of resuscitation steps once PPV is

Indications are(any 1 out of 3)

4. Hear rate < 100/min

5. Apnea or gasping

6. Persistent central cyanosis

Indications (1 out of 2) 3. Hear rate

< 100/min

4. Apnea or gasping

Heart rate Pulse oximetry Respiration

• Persistent central cyanosis is not mentioned in the indication for PPV; use pulse oximetry to assess oxygenation • Increase in HR most

57

started despite free flow oxygen

Heart rate Color Respiration

sensitive indicator of resuscitation efficacy (LOE5)

5) Oxygenation 5.1) Assessment of oxygenation

• Based on color • Pulse oximetry recommended for only preterm < 32weeks with need for PPV

• Based on pulse oximetry for both term and preterm in case of following Situations a. Anticipated need for resuscitation b. Need for PPV for more than few breaths c. Persistent cyanosis d. Supplementary oxygen

• Attach probe to right hand or wrist (measure pre-ductal saturations) • Attach neonatal probe before connecting it to machine • Recording of tracing may take 1-2 min • Pulse oximetry should not replace clinical assessment

5.2) Target saturation (pre-ductal)

Not defined Target SpO2 ranges provided as a part of algorithm

1min- 60-65% 2 min- 65-70% 3min- 70-75% 4min- 75-80% 5min- 80-85% 10min- 85-95% (same for both term and preterm)

6) Initial oxygen concentration for resuscitation in case of PPV

Term babies(≥ 37 weeks) • Start with 100% O2 during PPV • However if room air resuscitation is started supplemental O2 up to 100% should be given if no improvement within 90 seconds following birth • In case non availability of O2- start room air resuscitation

Term babies (≥ 37 weeks) • Start with room air (21%) • No improvement in heart rate or oxygenation as assessed by pulse oximetry- use higher concentration by graded increase up to 100% to attain target saturations • Use blender for graded increased in delivered oxygen concentrations

LOE-2 • Paradigm shift from 100% to 21% O2 for resuscitation of term babies needing PPV • Supplemental oxygen started at 90 sec from birth in case of no improvement • Use of blender and pulse oximetry is recommended for term babies also

Preterm babies(<32weeks)

Preterm(<32weeks) • Initiate resuscitation

• Preterm start with O2

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• Start with oxygen concentration somewhere between 21-100% • No specific concentration recommended • Advocates use of blender for graded increment or decrement of O2 • Pulse oximetry for targeting SPO2-85-95%

using O2 concentration between 30-90% • Titrate O2 concentration to attain SPO2 values recommended at different time points • Uses blended air oxygen mixture judiciously guided by pulse oximetry

concentration 30-90% and then increase or decrease • No evidence to give appropriate initial oxygen strategy for infants 32-37 weeks

7) Peripartum suctioning for neonates born through meconiumstained amniotic fluid

• No routine oropharyngeal and nasopharyngeal suction • Tracheal suction only in non-vigorous babies born through meconium stained amniotic fluid (MSAF) • Intrapartum suctioning for MSAF not advised

• No routine oropharyngeal and nasopharyngeal suction required • Tracheal suction of nonvigorous babies with MSAF still to be continued though evidence for the same is conflicting • Intrapartum suctioning for infants with MSAF , after delivery of head before delivery of shoulder not advised

• No evidence for or refuting tracheal suction even in non vigorous babies born through MSAF (LOE 4) • However no change suggested to existing practice • If tracheal intubation is unsuccessful or there is severe bradycardiathen proceed to PPV

8) Initial breath strategy Positive pressure ventilation (PPV)

• No specific recommendation for short or long inflation time • No specific PIP recommendation • No specific recommendation for PEEP • Guiding of PPV looking at chest rise and improvement in heart rate

• No specific recommendation for short or long inflation time as evidence is conflicting • PIP- for initial breaths 20- 25 cm H2O for preterm and 30-40 cm H2O for some term babies • PEEP likely to be beneficial for initial stabilization

• No specific recommendation for inflation time (LOE 1) • Addition of PEEP in preterm suggested (LOE 5)

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of preterm infants, if provided with suitable equipment (T-piece or flow inflating bags) • Guide the PPV looking at heart rate and oxygenation especially in preterm, chest rise less reliable • Pressure monitoring device facilitates consistent delivery of pressures without any proven clinical benefit • Routine monitoring of tidal volume not recommended

9) CPAP in delivery room

Suggested for preterm babies ( < 32 weeks) with respiratory distress

Spontaneously breathing preterm infants with respiratory distress may be supported with CPAP or ventilation as per local practice(Class IIB; LOE B)

• CPAP is now mentioned in the algorithm for persistent cyanosis or labored breathing after initial steps, • CPAP in term babiesno evidence to support or refute its use. • May be considered for preterm infants with respiratory distress

10) Airway management 10.1) Confirmation of endotracheal tube placement 10.2) Laryngeal mask airway

Exhaled CO2 detection is recommended except in cardiac asystole where direct laryngoscopy may have to be Done For near term and term

Exhaled CO2 detection is recommended except in cardiac asystole where direct laryngoscopy may have to be Done

Indications for endotracheal intubation are same as are recommendations for confirming its placement in trachea.

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infants > 2500g may be used with no definite mention of indications

LMA may be used for infants >2000g and ≥ 34 weeks in case bag and mask is ineffective and tracheal intubation is unsuccessful or not feasible(LOE 2)

LMA not recommended - in cases of me conium stained AF, during CCR and for drug administration

10) Airway management 10.1) Confirmation of endotracheal tube placement 10.2) Laryngeal mask airway

Exhaled CO2 detection is recommended except in cardiac asystole where direct laryngoscopy may have to be Done For near term and term infants > 2500g may be used with no definite mention of indications

Exhaled CO2 detection is recommended except in cardiac asystole where direct laryngoscopy may have to be Done LMA may be used for infants >2000g and ≥ 34 weeks in case bag and mask is ineffective and tracheal intubation is unsuccessful or not feasible(LOE 2)

Indications for endotracheal intubation are same as are recommendations for confirming its placement in trachea. LMA not recommended - in cases of me conium stained AF, during CCR and for drug administration

11) Upper airway interface

• Mask- rounded cushioned of appropriate size • Other alternative is anatomical shaped mask

• Evidence for anatomical shaped or rounded mask to maintain seal is conflicting (LOE 5) • PPV by nasal prongs superior to facial masks for providing PPV(LOE2)

Nasal prongs are an alternative way of giving PPV

12) Method of providing PPV

Bag mask ventilation Bag mask superior to mouth to mask or mouth to tube ventilation

In resource limited setting mouth mask (LOE 2)or mouth tube ventilation may be used(LOE 5)

13) Chest compression

• Ratio of compression 3:1 • Two thumb technique better than two finger technique • The compression is applied

• Ratio of compression 3:1 unless cardiac arrest is due to a clear cardiac etiology

No major changes in the guidelines and most recommendations are based on low level of evidence(LOE5)

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at the lower one third of sternum • The depth of compression should be one-third of the antero-posterior diameter of the chest

where ratio of 15:2 may be considered • Two thumb technique better than two finger technique • The compression is applied at the lower one third of sternum • The depth of compression should be one-third of the antero-posterior diameter of the chest

14) Drugs 14.1) Naloxone

Naloxone considered in case of infants born to mothers with history of opiod exposure within 4 hours of delivery and there is persistent respiratory depression even after restoration of heart rate and color by effective PPV

• Naloxone is not recommended as part of initial resuscitation in babies with respiratory depression. • Focus needs to be on effective ventilation

• Safety and long term effects on naloxone not established(LOE 5) • Naloxone is not indicated in delivery room.

15) Supportive care 15.1)Therapeutic Hypothermia

No sufficient evidence to recommend routine use of modest systemic or selective cerebral hypothermia after resuscitation in infants with suspected asphyxia Avoid hyperthermia in such cases

Therapeutic hypothermia (whole body or selective head cooling) recommended for infants ≥ 36weeks with moderate to severe hypoxic ischemic encephalopathy as per the protocol used in major cooling trials with provision for monitoring for side effects and

Lack of supporting evidence from resource-limited settings, need of intensive and multidisciplinary care during therapeutic hypothermia and established follow-up services after discharge limit the applicability in middle- and low-income countries

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long term follow up

15.2)Delayed cord clamping

Not recommended For uncomplicated births both term and preterm not requiring resuscitation – delay cord clamping by at least 1 minute

Delaying cord clamping for at least 1 min in all infants not requiring resuscitation at birth(LOE1)

16) Changes in ongoing care

After birth 3 types of care mentioned • routine care, • observational care and • post resuscitation care

Post resuscitation two types of ongoing care mentioned • routine care and • post resuscitation care

17) Withholding Resuscitation

• The guidelines needs to interpreted according to local policy In general withhold care for • Gestational age < 23 weeks • Birth weight <400 grams • Major chromosomal anomalies (e.g. Trisomy 13) • Anencephaly • The decision to this regard should be taken only after examining the baby after birth and with parental agreement

• The guidelines needs to interpreted according to local policy In general withhold care for • Gestational age < 23 weeks • Birth weight <400 grams • Major chromosomal anomalies (eg. Trisomy 13) • Anencephaly • The decision to this regard should be taken only after examining the baby after birth and with parental agreement

No change in the guidelines

18) Discontinuing care

If there is no detectable heart rate for >10 min despite adequate measures, it is appropriate to discontinue resuscitation measures.

If there is no detectable heart rate for >10 min despite adequate measures, it is appropriate to discontinue resuscitation measures

In situations of prolonged bradycardia with heart rate < 60 /min for > 10-15 min, there is insufficient evidence to make recommendation regarding

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continuation or discontinuation of resuscitation

19) Educational program to teach resuscitation

No mention of such a section

AHA/AAP NRP should adopt simulation, briefing-debriefing techniques in designing an educational program for acquisition and maintenance of skills necessary for effective neonatal resuscitation.

This recommendation is newly added to design NRP programme in a more effective manner.

Common Errors in Newborn Resuscitation

• Delivery room too cold for the baby • Non-preparation of equipment

• Doses of emergency drugs • No team leader is assigned

• Unprepared or non-skilled personnel • What drugs to give in what route of adminstration • Too much resuscitation/ too little resuscitation

• No need for ECG tracings to verify heart rate

Take home message

• Be prepared always • Be an NRP Provider

• Always update yourself

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PLENARY V

“Wound Care Assessment and Management”

RAMON O. RIBU, MD

Section Head, CTMAS & Wound Care,

Philippine Heart Center

Wound healing is a complex series of events that are interlinked and dependent on one another

. Acute wounds usually follow a well-defined process. In the past this model has been applied

to chronic wounds , but it is now known that chronic wound healing is different from acute

wounds. Wound bed preparation as a concept allows the clinician to focus systematically on all

of the critical components of a chronic woundto identify the cause of the problem and

implement care program to achieve a stable wound that has healthy tissue and well-

vascularized wound bed

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WOUND HEALING &

WOUND BED PREPARATION

Ramon O. Ribu, MD, FPCS, FPATACSI

Department of Cardiovascular Surgery & Anesthesia

Philippine Heart Center

BRIEF HISTORY

2000 B.C.

• Sumerians employed two modes of wound treatment.

Incantations

poultice

• The 1650 B.C. Edwin Smith Surgical Papyrus

describes at least 48 different types of wounds

• Ebers Papyrus, 1550 B.C.

relates the use of concoctions containing

honey (antibacterial properties)

lint (absorbent properties)

grease (barrier)

• Galen of Pergamum (120–201 A.D.)

doctor to the Roman gladiators

emphasized the importance of maintaining a moist environment

It took almost 19 centuries for this important concept to be proven scientifically

epithelialization rate increases by 50% in a moist wound environment when

compared to a dry wound environment

• Ignaz Philipp Semmelweis, a Hungarian obstetrician (1818–1865)

puerperal fever incidence

• Louis Pasteur (1822–1895)

the theory of spontaneous generation of germs

germs were always introduced into the wound from the environment

On a visit to Glasgow, Scotland, Lister noted that some areas of the city's sewer

system were less murky than the rest.

Discovered water from pipes that were dumping waste containing carbolic acid

(phenol) was clear.

In 1865, Lister began soaking his instruments in phenol and spraying the

operating rooms, reducing the mortality rates from 50 to 15%.

• 1876, Robert Wood Johnson

attended an impressive lecture by Lister in 1876 soon left the meeting and began

10 years of research

He developed antiseptic dressing in the form of cotton gauze impregnated with

iodoform.

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Since then, several other materials have been used to impregnate cotton gauze

to achieve antisepsis.

• The 1960s and 1970s led to the development of polymeric dressings.

• These polymeric dressings can be custom made to specific parameters:

o permeability to gases (occlusive vs. semiocclusive), varying degrees of

absorbency, different physical forms.

• Due to the ability to customize, the available range of materials that aid in wound care

has grown exponentially to include an ever expanding variety.

• Currently, the practice of wound healing encompasses manipulation and/or use of,

among others,

inflammatory cytokines,

growth factors,

and bioengineered tissue.

It is the combination of all these modalities that enables optimal wound

healing.

WOUND HEALING

Wound Depth Involvement

A. Epidermis

1. Stratum Corneum 3. Stratum Spinosum

2. Stratum Lucidum 4. Stratum Basale

B. Dermis

1. Papillary Layer

2. Reticular Layer

C. Hypodermis( SuperficialFascia)

D. Deep Fascia

E. Muscle

Normal wound healing follows a predictable pattern that can be divided into overlapping

phases:

PHASE 1: Hemostasis and Inflammation

PHASE 2: Proliferation

PHASE 3: Maturation and Remodeling

The cellular, biochemical, and mechanical phases of wound healing

A. The hemostatic / inflammatory phase.

Hemostasis precedes and initiates inflammation with the ensuing release of chemotactic factors

from the wound site

Exposure of subendothelial collagen to platelets results in platelet aggregation, degranulation,

and activation of the coagulation cascade.

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Cellular infiltration after injury follows a characteristic, predetermined sequence

PMNs are the first infiltrating cells to enter the wound site, peaking at 24 to 48h

A. The hemostatic / inflammatory phase.

Increased vascular permeability local prostaglandin release chemotactic substances such as

complement factors and interleukin-1

Latter inflammatory phases reflecting infiltration by mononuclear cells and lymphocytes.

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B. The proliferation phase.

The second phase of wound healing and roughly spans days 4 through 12

It is during this phase that tissue continuity is re-established. Fibroblasts and endothelial cells

are the last cell populations to infiltrate the healing wound, and the strongest chemotactic

factor for fibroblasts is PDGF.

Upon entering the wound environment, recruited fibroblasts first need to proliferate, and then

become activated, to carry out their primary function of matrix synthesis remodeling.

Matrix Synthesis Remodeling

Collagen Synthesis

Collagen, the most abundant protein in the body, plays a critical role in the successful

completion of adult wound healing.

Type I collagen is the major component of extracellular matrix in skin. Type III, which is also

normally present in skin, becomes more prominent and important during the repair process.

Collagen synthesis, as well as posttranslational modifications, are highly dependent on systemic

factors such as an adequate oxygen supply; the presence of sufficient nutrients (amino acids

and carbohydrates) and cofactors (vitamins and trace metals); and the local wound

environment (vascular supply and lack of infection). Addressing these factors and reversing

nutritional deficiencies can optimize collagen synthesis and deposition.

Proteoglycan Synthesis

Glycosaminoglycans comprise a large portion of the "ground substance" that makes up

granulation tissue.

The major glycosaminoglycans present in wounds are dermatan and chondroitin sulfate.

Fibroblasts synthesize these compounds, increasing their concentration greatly during the first 3

weeks of healing.

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C. The Maturation and Remodeling Phase

Begins during the fibroplastic phase, and is characterized by a reorganization of previously

synthesized collagen.

There is a net shift toward collagen synthesis and eventually the re-establishment of

extracellular matrix composed of a relatively acellular collagen-rich scar.

The deposition of matrix at the wound site follows a characteristic pattern:

fibronectin and collagen type III constitute the early matrix scaffolding;

glycosaminoglycans and proteoglycans represent the next significant matrix

components; and collagen type I is the final matrix.

Fibril formation and fibril cross-linking result in decreased collagen solubility, increased strength,

and increased resistance to enzymatic degradation of the collagen matrix. Scar remodeling

continues for many (6 to 12) months postinjury, gradually resulting in a mature, avascular, and

acellular scar.

The mechanical strength of the scar never achieves that of the uninjured tissue.

Epithelialization

This process is characterized primarily by proliferation and migration of epithelial cells adjacent

to the wound

The process begins within 1 day of injury and is seen as thickening of the epidermis at the

wound edge.

Marginal basal cells at the edge of the wound lose their firm attachment to the underlying

dermis, enlarge, and begin to migrate across the surface of the provisional matrix

Fixed basal cells in a zone near the cut edge undergo a series of rapid mitotic divisions,

and these cells appear to migrate by moving over one another in a leapfrog fashion until the

defect is covered.

The healing by epithelialization of superficial cutaneous wounds

Re-epithelialization is complete in less than 48 hours in the case of approximated incised

wounds, but may take substantially longer in the case of larger wounds, where there is a

significant epidermal/dermal defect.

Types of Wound Healing

1. Primary Intention

An incised wound that is clean and sutured closed is said to heal by primary intention.

2. Secondary Intention

Often, because of bacterial contamination or tissue loss, a wound will be left open to heal by

granulation tissue formation and contraction; this constitutes healing by secondary intention.

3. TERTIARY INTENTION

Delayed primary closure, or healing by tertiary intention, represents a combination of the first

two, consisting of the placement of sutures, allowing the wound to stay open for a few days,

and the subsequent closure of the sutures

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Classification of Wounds

Wounds are classified as either:

1. Acute

2. Chronic.

Acute Wounds

Acute wounds heal in a predictable manner and time frame.

The process occurs with few, if any, complications, and the end result is a well-healed

wound.

Surgical wounds can heal in several ways.

An incised wound that is clean and sutured closed is said to heal by primary intention.

Chronic Wounds

Chronic wounds are defined as wounds that have failed to proceed through the orderly

process that produces satisfactory anatomic and functional integrity or that have

proceeded through the repair process without producing an adequate anatomic and

functional result.

The majority of wounds that have not healed in 3 months are considered chronic.

The increased production of exudates that often accompanies increased microbial

load has been associated with the degradation of growth factors and matrix

metalloproteinases (MMPs) which subsequently affect cell proliferation and wound

healing .

In general, factors that adversely affect wound healing can be remembered by using the

mnemonic device DIDN'T HEAL, as follows:

D = Diabetes:

The long-term effects of diabetes impair wound healing by diminishing sensation and arterial

inflow. In addition, even acute loss of diabetic control can affect wound healing by causing

diminished cardiac output, poor peripheral perfusion, and impaired polymorphonuclear

leukocyte phagocytosis.

I = Infection:

Infection potentiates collagen lysis. Bacterial contamination is a necessary condition but is not

sufficient for wound infection. A susceptible host and wound environment are also required.

Foreign bodies (including sutures) potentiate wound infection.

D = Drugs:

Steroids and antimetabolites impede proliferation of fibroblasts and collagen synthesis.

N = Nutritional problems:

Protein-calorie malnutrition and deficiencies of vitamins A, C, and zinc impair normal wound-

healing mechanisms.

T = Tissue necrosis

resulting from local or systemic ischemia or radiation injury, impairs wound healing.

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H = Hypoxia:

Inadequate tissue oxygenation due to local vasoconstriction resulting from sympathetic

overactivity may occur because of blood volume deficit, unrelieved pain, or hypothermia,

especially involving the distal extent of the extremities.

E = Excessive tension on wound edges:

This leads to local tissue ischemia and necrosis.

A = Another wound:

Competition between several healing areas for the substrates required for wound healing

impairs wound healing at all sites.

L = Low temperature:

The relatively low tissue temperature in the distal aspects of the upper and lower extremities (a

reduction of 1-1.5°C [2-3°F] from normal core body temperature) is responsible for slower

healing of wounds at these sites.

Specific etiologies

1. Arterial insufficiency

2. Venous insufficiency

Patients with varicose veins or nonfunctional venous valves after deep vein thrombosis develop

ambulatory venous hypertension, that is, distal venous pressure remains elevated despite

ambulation. This constant venous hypertension seems to cause white cell and fibrin buildup,

which impairs capillary blood flow or traps growth factors. Macromolecules pass into the dermis

and eventually cause the hemosiderin deposition and brawny induration in the distal leg (gaiter

area) characteristic of chronic venous insufficiency.

3. Lymphedema

Although not typically a cause of ulceration, extremity ulcers may fail to heal because of

untreated lymphedema. Nocturnal leg elevation and elastic wraps or support hose are

appropriate adjuncts to the treatment of recalcitrant wounds in edematous extremities. For

advanced and nonresponsive lymphedema, complex decongestive physiotherapy is a useful

treatment option.

4. Neuropathy

Sensory neuropathy involving the feet may lead to unrecognized episodes of trauma caused by

ill-fitting shoes. This is compounded by motor neuropathy causing intrinsic muscle weakness

and spaying of the foot on weight bearing. The result is a convex foot with a rocker-bottom

appearance. Multiple fractures go unnoticed, until bone and joint deformities become marked.

This is termed a Charcot foot (ie, neuropathic osteoarthropathy) and is observed most

commonly in people with diabetes mellitus, affecting approximately 2% of persons with

diabetes.

5. Pressure (decubitus) ulcers

Pressure (decubitus) ulcers occur because of prolonged ischemia-producing external pressure,

usually to a soft tissue region overlying a bony prominence. Tissue ischemia results when

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external pressure exceeds capillary closing pressure (ie, 25-32 mm Hg in healthy individuals),

the minimum pressure that causes collapse of the capillary when applied to a capillary bed.

6. Neoplasms

Neoplasms strongly suggest malignancy in any chronic nonhealing wound, particularly if the

wound appeared to occur spontaneously.

7.Radiation damage

Gamma radiation and x-ray exposure cause a zone of stasis, in which local blood supply is

impaired by coagulative necrosis due to thrombotic occlusion of smaller arteries. Gamma and x-

ray radiation also spawn ionized oxygen that adversely affects DNA. The long-term result is

inhibition of regeneration of skin cells from dividing basal cells. This may cause recalcitrant

painful skin ulcers. The surrounding skin is atrophic, with atrophy of hair follicles and a paucity

subcutaneous fat.

8. Atheroembolism syndrome

Patchy areas of ischemia involving the feet, especially in the presence of palpable pedal pulses,

suggest the possibility of atheroembolism of plaque fragments from ulcerated, although

nonocclusive, proximal atherosclerotic plaques or from thrombi lining the wall of an infrarenal

aortic aneurysm.

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Impediments to Wound Healing

Devitalised / Necrotic tissue

Debris

Exudates

Slough

Biofilm

Wound Assessment

"Assess the whole person and not just the hole in the person" -Dr. Gary Sibbald

Wound Bed Preparation

The term «Wound bed preparation (WBP)» was first described by Falanga et al (2000)

defined as the global wound management plan to accelerate endogenous healing and

to enhance the effectiveness of advanced wound care products

The ultimate aim is to ensure formation of healthy granulation tissue resulting in

complete wound closure

The TIME framework means identifying essential elements for optimal wound bed

preparation and correcting abnormalities contributing to impaired wound healing.

The TIME framework (T= Tissue, non-viable or deficient / I= Infection or Inflammation

/ M= Moisture imbalance / E= Edge of wound, non-advancing or undermined) was

developed by Schultz et al in 2003 to provide a systematic approach to the management

of chronic wounds

Proper WBP

Reduction of bacterial bioburden in the wound bed

Removal of necrotic tissue and slough

Control of exudate

Management of cellular dysfunction and biochemical imbalance

3 Components of Local Care – DIM

Debridement

Infection and inflammation

Moisture balance

If wound bed preparation is optimised and healing is stalled, the additional

E or the edge of non-healing wounds represents the potential use of advanced active

therapies to stimulate healing.

Remember this, DIM before DIME

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WOUND ASSESSMENT

Wound Bed

Necrotic

Wound containing dead tissue. It may appear hard, dry and black. Dead connective tissue may

appear grey. Eschars with time may soften by autolysis and bacterial liquefacation. The

presence of dead tissue in wounds delays healing.

Sloughy

Slough is formed by an accumulation of dead cells in the wound exudate. It is light yellow in

colour and must not be confused with infected tissue and pus.

Granulating

Healthy red tissue, which occurs during the proliferative phase of healing. Firbroblasts migrate

to the wound to produce collagen fibres. The tissue is well vascularised and bleeds easily.

Epithelializing

Process by which the wound surface is covered by new epithelium, this begins when the wound

has filled with granulation tissue. The tissue is pink, almost white, and only occurs on top of

healthy granulation tissue.

Wound Measurement

Wound measurement is a vital aid to examining the healing process within a wound. Chronic

wounds should be measured 4 weekly (diabetic foot ulcers – weekly).

The wound should be measured at its greatest length and breadth:

The two measurements are then multiplied to give an approximate wound area in CM2. This

method can be unreliable where different professionals are assessing the same wound and also

where the shape of the wound is quite irregular.

Exudates

Exudate is produced by all acute and chronic wounds (to a greater or lesser extent) as part of

the natural healing process but may become more viscous and malodorous in infected wounds.

It plays an essential part in the healing process in that it:

Contains nutrients, energy and growth factors for metabolising cells

Contains high quantities of white blood cells

Maintains a moist environment for wound healing

Infection

Wound infection may be defined as the presence of bacteria or other organisms, which lead to

a host reaction. A host reaction can present as any one or combination of the following

signs:

Redness (erythema) around the wound

The production of large amounts of exudate or pus

A change in exudate colour

Malodour

A raised systemic temperature

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Localised pain

Localised heat

Lymphangitis

Delayed or abnormal wound healing

Wound breakdown

The appearance of fragile tissues which may bleed easily when touched or at the time of

a dressing change.

Wound Beds need to be assessed for:

• Granulation tissue (RED)

• Fibrin slough (YELLOW)

• Eschar (BLACK)

• Bone

• Tendon

• Other underlying structure

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WBP Components

1. Wound Etiology/Wound Cause:

– acute or chronic

– wound diagnosis (type)

– wound history

3. Local Wound Healing Trajectory

The “HEALABILITY” of the wound

cause is treatable

there is ADEQUATE blood supply

coexisting conditions or drugs that may affect healing

Determining Healability of Wound

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WOUND ASSESSMENT

What are the goals for this patient?

healing the wound

protecting the wound from further breakdown/infection

comfort

decrease in pain during dressing change

What is the patient's prognosis?

What is the patient's quality of life?

Is current pain control adequate?

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WOUND BED PREPARATION

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Types of Wound Debridement

Surgical/Sharp Debridement

Most expeditious form, but not always feasible due to: Pain Bleeding potential

Cost Lack of clinician expertise

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Autolytic Debridement

Highly selective process involving macrophage and endogenous proteolytic

enzymes which liquefy and separate necrotic tissue and eschar from healthy tissue.

Natural process is further enhanced by the use of occlusive and semi-occlusive dressings and those which interact to create a moist environment

Enzymatic Debridement

A less common method of debridement but effective in the removal of hard necrotic eschar where

surgical debridement is not an option. Exogenous enzymes are applied to the wound bed where they combine with the

endogenous enzymes in the wound to break down the devitalised tissue. Mechanical Debridement

Biological Debridement

Larval or Maggot Therapy

Larval therapy is a quick, efficient method of removing slough and debris from a

wound

Not all patients or staff find this debridement method socially acceptable

Sterile larvae secrete powerful enzymes to break down devitalised tissue without

destroying healthy granulation tissue (Thomas et al, 1998).

Osmotic Debridement

If debridement is effective, the T of TIME is removed and wounds can progress through the

remaining phases of wound healing.

Microbes and Chronic Wounds

z All chronic wounds are contaminated by bacteria.

z Wound healing occurs in the presence of bacteria.

z Certain bacteria appear to aid wound healing.

z It is not the presence of organisms but their interaction with the patient that determines

their influence on wound healing.

z Wound contamination: the presence of non-replicating organisms in the wound.

z All chronic wounds are contaminated.

z These contaminants come from the indigenous microflora and/or the environment.

z Most contaminating organisms are not able to multiply in a wound. (Ex. Most organisms

in the soil won‟t grow in a wound).

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Microbiology of Wounds

z The microbial flora in wounds appear to change over time.

z Acute wound; Normal skin flora predominate.

z S. aureus, and Beta-hemolytic Streptococcus soon follow. (Group B Streptococcus and S.

aureus are common organisms found in diabetic foot ulcers)

z After about 4 weeks

z Facultative anaerobic gram negative rods will colonize the wound.

z Most common ones= Proteus, E. coli, and Klebsiella.

z As the wound deteriorates deeper structures are affected. Anaerobes become more

common. Oftentimes infections are polymicrobial (4-5).

z Long-term chronic wounds oftentimes contain more anaerobes than aerobes.

z Aerobic gram-negative rods also infect wounds late in the course of chronic wound

degeneration. Usually acquired from exogenous sources; bath and foot water

z Ex. Pseudomonas, Acinetobacter, Stenotrophomonas (Xanthomonas).

z Organisms like Pseudomonas are not very invasive unless the patient is highly

compromised (ex. Ecthyma gangrenosum in neutropenic patients).

z These organisms are associated with marked wound deterioration due to endotoxin,

enzymes, and exotoxins.

z As the wounds go deeper and become more complex they can infect the underlying

muscles and bone causing osteomyelitis.

z Coliforms and anaerobes are associated with osteomyelitis in these patients. You also

see Staphylococcus aureus.

z Enterococcus and Candida are often isolated from wounds.

z Treating a patient for these organisms is only indicated if there are no other pathogens

present and the organisms are present in high concentrations (106 per gram of tissue)

z In summary: early chronic wounds contain mostly gram-positive organisms.

z Wounds of several months duration with deep structure involvement will have on

average 4-5 microbial pathogens, including anaerobes (see more gram-negative

organisms).

Dose of Bacteria

z Differs depending on the organism involved.

z Some organisms would need to be in high concentrations. (ex. Candida, Enterococcus)

z Various combinations of bacterial species result in more host damage (synergy)

z Example; Group B Streptococcus (S. agalatiae) and Staphylococcus aureus.

z Organisms that should be treated regardless of the numbers present.

z Beta-hemolytic streptococci, Mycobacteria sp., Bacillus anthracis, Yersinia pestis,

Corynebacterium diphtheriae, Erysipelothrix rhusiopathiae, Leptospira sp., Treponema

sp., Brucella sp., Clostridium sp., VZV, HSV, dimorphic fungi, Leishmaniasis.

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Bacterial Problems to Consider

z Streptococcus pyogenes

z Can result in necrotizing fasciitis or streptococcal toxic shock syndrome. Not very

common. Only about 520 cases per year of each condition.

z More common to see cellulitis and erysipelas after infection of a chronic wound.

z Clostridium tetani

z Contamination of chronic wounds by exogenous sources is common.

z Make sure your patients have gotten their tetanus vaccination.

z Erysipelothrix rhusiopathiae can infect chronic wounds. Associated with hog farmers

and people who fish.

z Mycobacteria marinum and M. ulcerans can infect chronic wounds. Think of people

who have aquariums, pools, go fishing, etc..

Virulence

z Factors an organism produces can result in host damage.

z Ex. Hyaluronidase (Streptococcus pyogenes), proteases (Staphylococcus aureus,

Pseudomonas aeruginosa),

z toxins (Streptococcus pyogenes, Staphylococcus aureus),

z endotoxin (gram negative organisms).

Wound Depth can result in different cases

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Host Resistance

z Host resistance is the single most important determinant in wound infection.

z Local and Systemic factors both play a role in increasing the chances a wound will

become infected.

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BIOFILMS

are complex microbial communities containing bacteria and fungi;

are relatively stable, three-dimensional communities of microbial cells encased in a

complex mixture of extracellular polymers.

are detrimental to wound healing and will hinder the process, but infection causes tissue

destruction

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BIOFILM FORMATION

Stage 1: Reversible Surface Attachment

Free-floating, or planktonic, bacteria encounter a submerged surface and within

minutes can become attached. They begin to produce slimy extracellular polymeric

substances (EPS) and to colonize the surface. The initial attachment is reversible.

Stage 2: Permanent Surface Attachment

As the bacteria multiply, they become more firmly attached (sessile) and differentiate,

changing gene expression patterns in ways that promote survival. This is usually the

result of a type of bacterial communication known as quorum sensing.

Stage 3: Slimy Protective Matrix

Once firmly attached, the bacteria begin to secrete a surrounding matrix known as

extracellular polymeric substance (EPS). This is a protective matrix or „slime‟. Small

bacterial colonies then form an initial biofilm

Effects of Biofilms

Bacterial biofilms are known to contribute to numerous chronic inflammatory diseases and

recent evidence suggests that biofilms also play important roles in impairing healing in chronic

wounds. Biofilms have high levels of tolerance to antibodies, antibiotics, disinfectants and

phagocytic inflammatory cells.

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HOW ARE BIOFILMS RELEVANT TO WOUNDS?

Biofilms are a major contributor to diseases that are characterised by an underlying

bacterial infection and chronic inflammation, eg. periodontal disease, cystic

fibrosis, chronic acne and osteomyelitis

biofilm cells have increased virulence and resistance to immunological defenses, and

decreased sensitivity to inhibitors such as antibiotics and antiseptics.

HOW QUICKLY DO BIOFILMS FORM?

within minutes > biofilms attach themselves

2 – 4 hours > form strongly attached microclonies

6 – 12 hours > develop initial EPS & become increasingly

tolerant to biocides, eg. Antibiotics,

Antiseptics, & Disinfectants

within 24 hours > rapidly recover from mechanical disruption

& reform mature biofilm

2 – 4 dayS > evolve into fully mature biofilm colonies that

are extremely resistant to biocides & shed

planktonic bacteria

HOW DO MATURE BIOFILMS PROTECT BATERIA?

Biofilms greatly enhance the tolerance of microorganisms embedded in the matrix to the

immune system, antimicrobials

and environmental stresses (eg. nutritional or oxygen limitation). This tolerance may approach

complete resistance to factors that would easily kill these same microbes when growing in an

unprotected, planktonic state.

THE ROLE OF WOUND CLEANSING IN WBP

WOUND CLEANSING is one of the basic principles of proper WBP

Usual irrigation solution include:

Normal Saline

Water

Antiseptics

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Advanced wound irrigation

Thorough wound cleansing with an advanced wound irrigation solution should be the

aim of every clinician as a prerequisite for normal wound healing and as an efficient

contribution to wound bed preparation by the removal of biofilm (Seipp 1999), slough

and necrotic tissue.

Although water may be used as a wound cleanser, and has not been seen to increase

the risk of infection or delay healing evidence is emerging that the combination of PHMB

with a surfactant (betaine) has an increased

ability to penetrate difficult-to-remove coatings, lifting debris, bacteria and biofilm from

the wound.

Surface tension is a parameter to measure cleansing efficacy.

The surface tension of PHMB + Betaine solution is LOWER than the surface tension of

water. This allows better removal of biofilm than water

Efficacy of various wound irrigation solutions against biofilms. Seipp HM, Hofmann S,

Hack A, Skowronsky A, Hauri A., ZfW 2005;4(5):160-163.

Conclusion: The results showed no decrease in the original biofilm load after

exposure to normal saline solution as well as Ringer‟s solution, while the

surfactant polyhexanide solution (Prontosan® Wound Irrigation Solution)

achieved a significant reduction (p<0.001) of the biofilm by 87%.

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Moisture Balance

New guidelines highlight that rapid healing of the wound is best achieved by providing a moist

environment, which accelerates the rate of wound repair by up to 40%

SELECTION OF Wound Dressings

Specific product focus for each TYPE of wound at every PHASE of wound healing.

Moist wound healing has been the evidence based /best practice approach since Dr. George

Winter first published his studies in 1962.

Providing a balance is essential for necessary healing

• Maintains optimal temperature

• Decreases infection potential

• Decreases patient pain at dressing change

• Decreases TRAUMA to the fragile granulating tissue of the wound bed

• Moist = moist like your eyeball

An ideal dressing should keep the wound bed moist, protect periwound skin from maceration,

protect from secondary infection, be free of toxic components, and not cause trauma upon

removal. To enhance healing, the ideal dressing should provide thermal insulation and should

be left intact for as long as possible.

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Wound Dressing

Note:

It is important to remember to reassess the wound each time you change the dressing.

Documentation needs to be specific:

measure and describe the wound.

Dressing selection/treatment should also be clearly documented.

The word is GENTLY.

Minimize wound trauma during wound cleansing.

Normal Saline is the agent of choice.

No betadine, chlorohexadine, or Hydrogen

peroxide.

Choice of Dressings

It should be recognised that a wound will require treating differently at various stages of its

healing. No dressing is suitable for all wounds.

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Following careful selection of the appropriate management plan for the patient, the wound

assessment tool should be used to monitor the progress of the wound through to its healing

stage.

Guideline statement

Criteria for Choosing a Dressing In Order of Importance (Miller & Collier, 1997)

1. Choose a dressing that maintains a moist environment at the wound/dressing interface.

(The only possible exceptions are peripheral necrosis secondary to arterial disease.

2. Choose a dressing that is able to control (remove) exudate. A moist wound environment is

good, a wet environment is not beneficial

3. Choose a dressing that does not stick to the wound and cause trauma on removal

4. Choose a dressing that protects the wound from the outside environment

5. Choose a dressing that will aid debridement if there is necrotic or sloughy tissue in the

wound (caution withischaemic lesions)

6. Choose a dressing that will keep the wound close to normal body temperature

7. Choose a dressing that is acceptable to the patient

8. Choose a dressing that is cost-effective

9. Diabetes – choose a dressing that will allow frequent inspection

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Important Note:

A single product is unlikely to be suitable for a particular wound throughout the wound healing

process. Regular re-assessment of the wound is essential together with documentation to

support rationale for change of dressing.

Communication between the acute/community setting and joint visits with other disciplines aid

holistic assessment and promote multidisciplinary team approach to wound care.

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Application of Bioengineered Skin Substitutes

1. Apligraf (Organogenesis; Novartis) is a bilayered skin substitute produced by combining

bovine collagen and living cells derived from tissue-cultured human infant foreskins. One study

of diabetic foot ulcers demonstrated 12-week healing rates of 39% for patients who received

only standard wound care versus 56% for those who were treated by application of an Apligraf

after a period of standard wound care.

2. Dermagraft (Smith & Nephew, Inc) is human fibroblast-derived dermal

substitute manufactured by seeding dermal fibroblasts onto a 3-dimensional

bioabsorbable scaffold. It has been marketed for use in the treatment of diabetic foot ulcers,

venous ulcers, and pressure sores. A clinical trial showed improved healing rates in diabetic foot

ulcers.

4. Oasis (Healthpoint, Ltd), a relatively new product, is a xenogeneic acellular collagen matrix

derived from porcine small intestinal submucosa in such a way that an extracellular matrix

and natural growth factors remain intact. This provides a scaffold for inducing wound healing.50

Do not use this in patients with allergies to porcine materials.

5. Cultured epithelial autograft (Epicel; Genzyme Tissue Repair, Cambridge, Mass) is an

epidermal replacement that is grown in a tissue culture from a skin biopsy taken from the

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recipient and is cocultured with mouse cells. Preparation of the graft requires about 2 weeks of

culture time.

Consider other topical agents

Topically applied platelet-derived growth factors have a modestly beneficial effect in promoting

wound healing.

1. Becaplermin gel 0.01% (Regranex), recombinant human platelet-derived growth

factor (PDGF) that is produced through genetic engineering, is approved by the US

Food and Drug Administration (FDA) to promote healing of diabetic foot ulcers. Regranex

is contraindicated in persons with known skin cancers at the site of application. Freeze-dried

platelet-rich plasma has shown promise in a recent animal study.

2. Collagenase : Collagen comprises a significant fraction of the necrotic soft tissues in chronic

wounds. The enzyme collagenase, which is derived form fermentation of Clostridium

histolyticum, helps remove nonviable tissue from the surface of wounds. However,

collagenase is not a substitute for an initial surgical excision of a grossly necrotic wound.

Pain

The pain associated with chronic wounds is often underestimated. In over 50% of cases, nurses

recording of patients‟ pain differed from self-reporting. In most of these cases, the nurses had

underestimated the patients‟ pain.

Pain assessment tools have many advantages:

Patient has a more active role in dealing with their pain The patient may feel that their pain is being taken seriously The tool often prompts more effective pain relieving measures, as documented

evidence exists. PERIWOUND AREA

Surrounding tissues may present as: healthy macerated

dry/flaky eczematous

blue/black discolouration oedema

erythema cellulitis

The surrounding skin should be examined carefully as part of the process of assessment and

appropriate action taken.

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NUTRITIONAL ASPECTS OF WOUND HEALING

Nutritional status plays a critical role in the wound healing process. Neglecting the nutritional

health of the individual may totally compromise all wound management to be carried out.

(Wallace, 1994)

Optimal Nutrition Helps To Maintain Immune Competence.

THE ESSENTIAL NUTRIENTS FOR WOUND HEALING

Protein, Vitamin C, B Complex and A, Zinc, Iron and Copper are essential for wound healing.

In addition to these nutrients, it is essential that adequate energy/calories are obtained from

fats and carbohydrates to prevent tissue protein being used as a source of energy.

PROTEIN

Requirements: 1.2 – 2.0g protein/kg/24h

Protein is required for healing tissues. Without adequate protein normal protein synthesis and

wound healing are inhibited. The immune response is diminished and there is a delay in matrix

formation.

Protein Sources:-

Meat, fish, eggs, milk, cheese, yoghurt, pulses and nuts.

Nutritional sip feeds will provide important sources of protein and other nutrients if dietary

intake is inadequate.

ENERGY

Requirements: 30-40 Kcal/kg/24h

An adequate energy/calorie intake is essential in order to prevent dietary and tissue protein

being used as a source of energy rather than for wound healing.

Energy Sources:-

All foods provide energy and preserve tissue protein.

Carbohydrate sources – bread, potatoes, breakfast cereal, rice and pasta, oils, spreads, butter,

margarine, fried foods.

Fat sources – oils and fats, butter, margarine, fried foods.

VITAMINS

Vitamin C

Requirements: A minimum of 60mg vitamin C.

Vitamin supplements from 200 mg – 1g per day are sometimes recommended [Taylor, 1974],

however excessive doses may cause renal stones [Morton, 1995].

Vitamin C is required for collagen synthesis and aids iron absorption.

Vitamin C is not stored in the body with patients rapidly becoming deficient. Supplements may

be necessary.

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Vitamin C Sources:- Citrus fruits and juices, blackcurrant juice drinks and fruit squashes fortified

with vitamin C tomato juice, all fruit and vegetables.

MINERALS

Zinc

Deficiency is associated with poor wound healing.

Zinc is required for collagen synthesis, epithelialization and cell proliferation.

Zinc supplements have been found to improve the healing of leg ulcers where zinc deficiency is

identified.

However, where there is no deficiency excess zinc can impair healing (Wells, 1994).

Zinc sources:- Liver, meat, fish, eggs, pulses including baked beans, wholegrain cereals.

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PLENARY VI

“Palliation and Spiritual Care: Phenomenology Approach in Critical Care”

RUDOLF CYMORE KIRBY P. MARTINEZ, MAN, RP-RN, CAA, LMT,

CSTP, PhD (c)

Complementary & Alternative Therapy Nurse Practitioner,

Pain Management Clinician and Staff Nurse

Philippine Children‟s Medical Center

"OF SHADOWS AND BUTTERFLIES": SITUATING THE ROLE OF PHENOMENOLOGY IN

CRITICAL CARE THRU THE LENS OF FILIPINO NURSE'S SPIRITUALITY

This presentation situates the role of phenomenology in the critical care setting thru the lens of

the nurse's daily mundane experiences with death and dying process. It will explore how

phenomenology, both as an approach and an attitude, can provide an immense wealth of

qualitative "evidence" which will inevitably inform their practice as critical care nurses. As a

subsequent example, this presentation will provide a glimpse of the rites and rituals that nurses

associate with the death and dying process, reflected upon thru the phenomenological

approach. These rites and rituals will be viewed and appreciated from the level of being a

simple personal experience to that of being a part of a uniquely Filipino cultural consciousness.

Lastly, this presentation will explore how these insights may help nurses develop their

competence as a professional and compassion as a human being.

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“OF THE SHADOWS AND BUTTERFLIES”

PHENOMENOLOGY IN CRITICAL CARE

Objectives:

• Familiarize with Phenomenology

• Situate Phenomenology in Critical • Care Setting

• Understand Filipino Spirituality • through Phenomenology

Phenomenology

The Study of a Phenomenon

Phenomenology:

“Bridges the gap between what is familiar in our worlds and what is unfamiliar” – Gadamer

“Prime intent is to describe and explore the meaning and essence of unconsolidated henomena

as lived experiences” – Speziale

REALITY PHENOMENON

Phenomenology is based on the assumption of the meaning of Reality

Reality is on People

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“Researcher's task is to understand reality as it is actively and consciously constructed by

subjects” – Alfred Schutz

Phenomenological Research

Core Characteristic

rigorously descriptive

uses the phenomenological reductions

explores the intentionality

discloses the essences through the use of

imaginative variation

Branches of Phenomenology

• Genetic

• Realistic

• Descriptive

• Hermeneutic

• Phenomenology

• Naturalistic

• Existential

• Generative Historicist

Descriptive Interpretative Descriptive Interpretative

Epistemology (question of knowing) Ontology (question of experiencing and

understanding)

Human share consciousness Human share culture

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Data speaks for itself Interpreter participate in making

data

Bracketing defending objectivity Hermeneutic circle (co-creation,

preunderstanding)

Historicality:

“A person‟s history or background, includes what a culture gives a person from birth and is

handed down, presenting ways of understanding” – Heidegger

“To be human was to Interpret” - Heidegger

Heideggerian Assumptions - Benner (1994)

• Human are social dialogical being

• Understanding is always before us

• Interpretation presupposes a shared understanding between the researchers & co-

researchers

• Interpretation involves the interpreter

“Language is the universal medium in which understanding occurs. Understanding occurs in

interpreting” – Gadamer

“Understanding and interpretation are bound together and interpretation is always an evolving

process, thus a definitive interpretation is likely never possible” – Annells

What do we want to understand in Interpretative Phenomenology?

• The experiences of people

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• The meanings of their experiences • The insight from those meanings

• Your journey in understanding what you • Understood

Phenomenology is both a Research Approach and an Attitude

Phenomenology Contextualize Reality

Makes Understanding Culturally Sensitive

“We cannot change anything until we accept it. Condemnation does not liberate, it oppresses.”

– Carl Jung

Critical Care Setting is Rich in Phenomenon that

could be explored though Phenomenology

Such as the MeSuch as the Meeting of Healing and Suffering

“Healing Through Suffering

Suffering Through Healing”:

The World of Pediatric

Cancer Nurses

Research Approach

Interpretative Phenomenology - Bridge the gap between what is known & unknown

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Selection of Co-Researchers

• Five Co-Researchers

• Criterion Sampling

Preset Criteria

• Willing to describe and articulate their experiences • Currently working at a pediatric cancer ward with al least 2 years of

experience in the said field

Ways of Gathering the Experiences

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Madugo” (Bloody): The Insignia of PCN

• Source of Distinguished Identity • Blood if Life, Blood Transfusion is • Transmission of Life • Life of their Patient is at their Hands • Blood Culture Reflected in Language

“Toxic”: Poison of Overindulgence

• Encapsulate the World of a PCN • Beyond Optimum, Things will be Toxic,

i.e. Chemotherapy, Duty, Attachment

• Toxicity Consumes One‟s Being, Blur the • Boundaries of Things • Toxicity is an Interplay of Time and Space

“Paruparo” (Butterflies): On Death and Dying

• Inseparable and Imminent Reality

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• Death Mask: Stoic, Emotionally Detached • Depersonalized Death: Dying Body, Living Spirit

• To be a PCN is to Embrace the “Paruparo” • Living Everyday as if it‟s Their Last

• Messenger, Soothsayer & Creator

Thematic Embodiment: Eidetic Insight

• Is a paradox of suffering and healing • Disparity of meanings and the seemingly polarity of things are but two sides of the coin,

opposite but in unity and can never be separated

• There can be no healing without suffering nor suffering without healing

Symbolic Representation

YinYang = Unity of Opposite, Inseparability of Healing & Suffering

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Red = Blood, Life, Healing

Black = Toxicity, Death, Suffering

Cross = End & Beginning of Life

Critical Care Setting is Rich in Phenomenon that could be explored though Phenomenology

Such as the Experience of Death and Dying

Unarmed:

Experiences of Seeing Death and Dying Among Filipino Nurses Working with Children

“…nurses shall collaborate with other health care providers for the curative, preventive, and

rehabilitative aspects of care, restoration of health, alleviation of suffering, and when recovery

is not possible, towards a peaceful death…” - RA 9173 Sec. 28

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Death and Dying is a Normal Phenomenon Among Hospital Nurses

Nurses Tend to Shy Away on the Topic of Death and Dying

Both Taboo and Less Explored

Shrouded in Secrecy and Mystery

What Insight maybe derived from Filipino Nurses Working with Children‟s

Experiences of Death and Dying

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Interpretative Phenomenology –

Bridge the gap between what is known & unknown

Five Co-Researchers

Criterion Sampling

Preset Criteria

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•Willing to describe and articulate their experiences

•Currently working at a pediatric ward with at least two years of experience in the said

field

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“Distance”: Fear of Death

• Pangamba (Dread) • First experience of Death

• Distancing oneself from Death • Patient is not seen as someone close to our heart

“When you know they have cancer, it‟s a different feeling, you‟ll pity them… when they have

cancer you know they‟ll eventually die, its inevitable”

“Detachment”: Fear of Dying

• Pag-aagam-agam (Uneasiness)

• Masked: Emotional Detachment

• General Feeling of Awkwardness

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• “job description” type of care

• Keeping one‟s self intact

“I‟ll see them as just my patients, I detached myself from them since I‟m on the verge of

crying… have you tried doing CPR while crying? They (children) are good people then they‟ll die

at your hand, on your duty, on your shift…”

“Depersonalized”: Fear for Oneself

• Dalamhati (Grief) • Repeated Experience of Death and Dying

• Emotional Callousness

• Accepting Death as Inevitable • Wear on or Wear out

“I thought I‟ll be closer to patient (as time goes by) but now I realized that instead, I am

becoming calloused… I feel nothing even pity even if the patient have nothing, even if he is an

only child… I feel nothing ”

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Interwoven work of life and death

Unarmed

Paradox of Closeness

Multi Layered Spectrum of Meaning: Loosing the Child to Loosing one‟s Touch of Humanity

Symbolic Representation

The Weeping Cherub

• Lost of the child • Touch of Humanity

• Hardened Persona

• Puer • Connection

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Context: Filipino Consciousness

Cultural Values Inform our

World View which Affect

How We Appreciate Things

KAPWA

SHARED IDENTITY (Shared Inner Self, “The other person is also yourself”)

• the core of Filipino psychology, it is

humaneness at the highest level

• implies unique moral obligation to treat

one another as equal fellow human beings

Treat the other person as you treat yourself

because the other person is also yourself

PAKIRAMDAM

(Knowing Through Feeling or Tacit Knowing; Participatory Sensitivity)

• A unique social skill inherent in Filipino personhood

• The need for openness and basic trust is a precondition for this active process of sensing

subtle cues

FILIPINO PROXEMICS

• To be alone a German needs four thick walls which shut off all light and sound from the

outside.

• A Japanese needs only thin paper screens

• A Filipino does not need a physical structure to spend time alone. All that is needed is for him

to stay in a corner and keep quiet.

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PHENOMENOLOGY

Place Prime Importance of Human

Experience as a Source of Valuable

Insight to Inform Our Practice

Brings Back Humanity to Nursing

Research and Practice

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PLENARY VII

“Empowerment of Nurses through a Career Progression Program”

HON. MARCO ANTONIO STO. TOMAS, RN, MAN

Member, Board of Nursing

Chair, Council for Nursing Advancement,

Recognition & Specialization

The International Scene

In 1992, the Philippines, together with the governments of Brunei, Darussalam, Republic of

Indonesia, Malaysia, Republic of Singapore, Kingdom of Thailand, and the Socialist Republic of

Vietnam were all signatories to the DECLARATION which provided that ASEAN shall move

towards a higher plane of economic cooperation to secure regional peace and prosperity and

further declared that the ASEAN Free Trade Area (AFTA) shall be established in the region.

This signaled the beginning of globalization which among others aimed to provide long-term

growth and development and enhance productivity, efficiency and global competitiveness of

professionals; promote opportunities; and to ensure delivery of better professional services.

This event in global history was geared to realize:

1. Liberalization of the Practice of various Professions, Nursing being one of these

2. Elimination of Discriminatory Practices

3. Institution of Deregulatory Policies

4. Provision of Mutual Recognition Measures

5. Harmonization and Standardization of Qualifications for Examination and Licensure as

well as Regulatory Requirements Pursuant to International Agreements

As a result of the 1992 Singapore ASEAN Agreement, ASEAN Member States pursued

further exploration of measures on border and non-border areas of cooperation to supplement

and complement the liberalization of trade pursuant to the Framework Agreement on Enhancing

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ASEAN Economic Cooperation. Member Economies also recognized that intra-ASEAN economic

cooperation will secure a liberal trading framework for trade-in services which would strengthen

and enhance trade- in services among ASEAN Member States, and they committed to the rules

and principles of the General Agreement on Trade-in Services (GATS) which aims to eventually

permit the Liberalization of Trade-in Services between or among the parties to an economic

integration agreement. This moreover affirmed that ASEAN Member States shall extend to one

another preference in trade-in services.

There was also the Uruguay Round of Talks and GATS. The General Agreement on Trade in

Services (GATS) was negotiated in the first set of multilaterally-agreed and legally-enforceable

rules and disciplines ever negotiated to cover international trade-in services. These Agreements

covered (1) a framework of general rules and disciplines, (2) annexes addressing special

conditions relating to individual sectors, and (3) national schedules of Market Access

commitments. These schedules like tariff schedules under the GATS are an integral part of the

agreement. A Council for Trade in Services oversees the operation of this agreement.

And there was the APEC and its BOGOR Declaration. Under this declaration, the Asia-Pacific

Economic Cooperation (APEC) member economies committed themselves to achieving free and

open trade-in services by 2010/2020. APEC members should begin to develop programs on

services for incorporation into their individual action plans. In some cases, action plans dealing

with services will inevitably need to refer to investment issues, since comercial presence is an

important means of delivering services abroad. For this reason, work on trade services will

need to be coordinated with work on free and open investments being done by APEC

Investment Experts. APEC‟s work best focused on major impediments to trade services and on

removing these impediments.

Come 2015, Filipino Professionals, especially nurses, are to witness the

beginning effects of all these international commitments signed by the Government

of the Republic of the Philippines.

National Scene. How has the Philippine Nursing Sector prepared for the impact of

globalization?

The practice of a profession like Nursing in the Philippines is governed by a professional

regulatory law which was enacted by the legislative body/congress pursuant to the Police

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Powers and Parens Patria of the State, as enshrined in the Philippine Constitution, to protect

the life, health, property, and welfare of the people via possession of the adequate levels of

knowledge, skills and competence, and of good moral character (integrity) by the

registered/licensed professional or the professional nurse. Every professional Regulatory law

(PRL) is to be administered and enforced by a Professional Regulatory Board (PRB) such as the

Board of Nursing.

In 1996, anticipating that the W.T.O.-ASEAN-AFAS-AFTA Liberalization of Trade-in Services will

take full effect by 1998 and the W.T.O.-APEC-GATS Liberalization of Trade-in Services having

adopted 2010/2020 as their target, then Board of Nursing through its Chairman Dr. Aurora

Yapchiongco, tasked a core group to carefully study the possibility of putting in place a

credentialing program for the nursing profession in pursuit of the need to prepare for global

competition, higher productivity, and better quality nursing products in order to access the

world market via APEC/GATTS. This move paved the way for the promulgation in February 18,

1999 of Board Resolution No. 14 which ruled for the adoption of a National Nursing Specialty

Certification Program. This was consequently followed by Board Resolution No. 24, series of

1999 which incorporated some amendments thereto. The first NSC Council was inducted into

office during the BoN Chairmanship of Hon. Corazon de la Pena. Nursing history will tell us that

these events happened between the legal-life of Republic Act 7164 passed in 1991 and upon its

repeal and implementation of R.A. 9173 passed in the year.

It is also worth recognizing that in 2002 the Association of Nursing Service Administrators or

ANSAP “voluntarily” set into motion its so-called Career Pathways for Nurse Practitioners as

private organizational initiative designed to give R.Ns under its organizational sphere of

influence the opportunity for career development within an acceptable framework which may

facilitate possible promotion in a clinical ladder that expected the professional nurse to assume

increasing responsibilities and rewards. This model and that of Patricia Benner‟s framework and

mechanisms are worthy of adaptation in as much as these models are very much in sync with

globally recognized and utilized mechanisms of advancement not only in theory but in practice

and the Board of Nursing sees no impediment for its legal adaption.

With the issuance of EXECUTIVE ORDER NO. 83, Series of 2012 by President Benigno S.

Aquino “Institutionalizing the Philippine Qualifications Framework (PQF)” as THE national policy

that describes the levels of educational qualifications and sets the corresponding standards for

qualification outcomes and which became effectivity last 1 October 2012, the Philippine Nursing

Sector MUST navigate effectively amidst a multitude of pressing socio-economic and political

events in Philippine Nursing history and where all the more a National Nursing Career

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Progression Program (NNCCP) is more than relevant in achieving local upscaling of

competencies and building further our international competitive advantage.

Today we feel all the more that what our former PRC Board of Nursing started in the 90‟s as

the Nursing Specialty Certification Program is at best our “unfinished business” in the pursuit of

professional relevance, quality, and global comparability and competitiveness, and excellence.

Hence our revitalized effort contained in the National Nursing Career Progression Program

(NNCCP) comes with a more unified and harmonized direction in keeping with the State Policy

of promoting “better career prospects and a dignified existence for our Filipino

nurses” (R.A. 9173 – Statement of Policy).

Indeed the CCNAPI‟s call to STAND T.A.L.L. (Together Advance in Learning and Life) is very

timely as the agenda that all organized Philippine Nursing Groups must undertake is exactly

this, no more and no less if we wish to achieve our vision in Philippine Nursing of being the

BEST FOR THE FILIPINOS AND THE CHOICE OF THE WORLD.

Empowerment of Nurses Through a Career Progression Program

OBJECTIVES:

At the end of this talk, participants shall have gained the necessary start-up understanding and

appreciation of the policy-directions of government through the Professional Regulatory Board

of Nursing in leveling-up and keeping the Philippine Nursing Profession nationally relevant but

globally comparable and competitive.

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This plenary talk shall focus on:

1. Present policy-framework/s which sets in motion the over-all and over-arching national

directions of setting standards in education and training, technical and professional practice,

and quality assurance measures for our Philippine Human Resources. This covers review of

relevant mandates e.g.:

1.1 E.O. No. 83 – Institutionalizing a Philippine Qualifications Framework (PQF)

and its IRR, and

1.2 BON Resolution No. 22, Series 2009 Providing for a National Nursing Career

Progression Program for Filipino Nurses which covers NOT ONLY nursing

specialties but General Nursing Practice as well.

2. Reiterate the challenge of putting in place a national machinery which pursues measures

towards professional competitiveness upscaling targeting a more prepared Philippine Nursing

Workforce in our country especially in the light of upcoming MRA negotiations in the ASEAN and

EU Communities.

Historical Brief

In 1992 – the following “economies” signed a DELCARATION which provided that ASEAN

shall move towards a higher plane of economic cooperation to secure regional peace and

rosperity and further declared that the ASEAN Free Trade Area (AFTA) shall be established

in the region.

1. Philippines 2. Brunei, Darussalam

3. Republic of Indonesia 4. Malaysia 5. Republic of Singapore

6. Kingdom of Thailand 7. Socialist Republic of Vietnam

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This signaled the beginning of globalization which among others aimed to provide long-term

growth and development and enhance productivity, efficiency and global competitiveness of

professionals; promote opportunities; and to ensure delivery of better professional services

Historical Brief

This event in global history was geared to realize:

Liberalization of the Practice of various Professions, Nursing being one of these (others incl. Medicine, Dentistry, Accountancy, Engineering, Architecture,

Agriculture) Elimination of Discriminatory Practices

Institution of Deregulatory Policies Provision of Mutual Recognition Measures (MRAs) Harmonization and Standardization of Qualifications for Examination and Licensure as

well as Regulatory Requirements Pursuant to International Agreements

Historical Brief

As a result of the 1992 ASEAN Agreement, ASEAN Member States:

1. pursued further exploration of measures on border and non-border areas of cooperation

to supplement and complement the liberalization of trade pursuant to the Framework Agreement on Enhancing ASEAN Economic Cooperation;

2. Member Economies also recognized that intra-ASEAN economic cooperation will secure a

liberal trading framework for trade-in services which would strengthen and enhance trade-in services among ASEAN Member States; and

3. they committed to the rules and principles of the General Agreement on Trade-in Services (GATS) which aims to eventually permit the Liberalization of Trade-in Services between or among the parties to an economic integration

agreement; and 4. that this affirmed that ASEAN Member States shall extend to one another

preference in trade-in services.

There was also the Uruguay Round of Talks and GATS. This GATS was negotiated in the first

set of multilaterally-agreed and legally-enforceable rules and disciplines ever negotiated to

cover international trade-in services. These Agreements covered:

(1) a framework of general rules and disciplines,

(2) annexes addressing special conditions relating to individual sectors, and

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(3) national schedules of Market Access commitments. These schedules like tariff

schedules under the GATS are an integral part of the agreement. A Council for Trade in

Services oversees the operation of this agreement.

And there was the APEC and its BOGOR Declaration. Under this declaration:

(1) the Asia-Pacific Economic Cooperation (APEC) member economies committed

themselves to achieving free and open trade-in services by 2010/2020;

(2) APEC members should begin to develop programs on services for incorporation into

their individual action plans;

(3) In some cases, action plans dealing with services will inevitably need to refer to

investment issues, since comercial presence is an important means of delivering services

abroad. For this reason, work on trade services will need to be coordinated with work on free

and open investments being done by APEC Investment Experts;

(4) APEC‟s work best focused on major impediments to trade services and on removing

these impediments.

BY 2015 -

The Philippines will witness the beginning effects of all the international

commitments signed by the Government of the Republic of the Philippines.

In 1996, anticipating that the W.T.O.-ASEAN-AFAS-AFTA Liberalization of Trade-in Services will take full effect by 1998;

And as the W.T.O.-APEC-GATS Liberalization of Trade-in Services adopted 2010/2020 as their target, then Board of Nursing Chairman Dr. Aurora Yapchiongco tasked a core group to carefully study the possibility of putting in place a credentialing program for the

nursing profession in pursuit of the need to prepare for global competition, higher productivity, and better quality nursing products in order to access the world market via

APEC/GATTS This move paved the way for the promulgation in February 18, 1999 of Board

Resolution No. 14 which ruled for the adoption of a National Nursing Specialty

Certification Program. This was consequently followed by Board Resolution No. 24, series of 1999 which incorporated some amendments thereto. The first NSC

Council was inducted into office during the BoN Chairmanship of Hon. Corazon de la Pena. Nursing history will tell us that these events happened between the legal-life of Republic Act 7164 passed in 1991 and upon its repeal and implementation of R.A. 9173

passed in the year 2000.

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In 2002 the Association of Nursing Service Administrators of the Philippines took the initiative of establishing/setting into motion a Career Pathway for Nurse Practitioners Program designed to give RNs the opportunity for career development within an acceptable framework which may facilitate possible promotion within a clinical

ladder that expected the professional nurse to assume increasing responsibilities and rewards.

This model and that of Benner‟s conceptual framework and mechanisms are worthy of

adaptation in as much as these are by now globally recognized and utilized not only in theory but in practice and the current Board of Nursing sees no impediment for its legal adaption. Hence, BON Resolution No.22, series of 2009 came into being

Institutionalizing a National Nursing Career Progression Program (NNCPP) adhering to the State Policy of promoting “better career prospects and a dignified existence for our Filipino nurses” (R.A. 9173 – Statement of Policy), Like any professional sector, navigating through a multitude of pressing socio-economic and political events in our country we can rightfully say that during

this part of our Nursing History, THIS IS YET AN “UNFINISHED BUSINESS” in the pursuit of professional relevance, quality, and global comparability and

competitiveness, and excellence… Especially in the light of E.O. 83, Series 2012

EXECUTIVE ORDER NO. 83,

Series of 2012

“Institutionalization of the Philippine Qualifications Framework”

Date of Effectivity : 1 October 2012

Implementing Rules and Regulations of E.O. No. 83

Date of publication: 28 December 2012

PQF

Is the national policy that describes the levels of educational qualifications and sets the

corresponding standards for qualification outcomes

Competency-based

Labor-market driven Assessment based qualification recognition

COVERAGE

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All sectors, levels and modes of delivery of the Philippines‟ tri-focalized education system: basic education, technical vocational education and training and higher

education; and All institutions and systems which provide trainings, specializations, skills and

competencies, professional experience or through lifelong learning

OBJECTIVES

Establishes national standards and level for OUTCOMES of education, training, specialization, skills and competencies

Provide national regulatory and QUALITY ASSURANCE arrangements for education and training

Support the development and maintenance of PATHWAYS AND EQUIVALENCES which provide access to qualifications

Supports individual LIFELONG LEARNING goals by providing the basis for individuals

to progress through education and training Aligns the PQF with international qualifications framework to support the national and

international mobility of learners and workers through increased RECOGNITION of the

value and comparability of Philippine QUALIFICATIONS

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PQF NATIONAL COORDINATING COMMITTEE

Chairman : Secretary, Department of Education

Members : Secretary, Department of Labor and Employment

Director-General, Technical Education and Skills

Development Authority

Chairperson, Commission on Higher Education

Chairperson, Professional Regulation Commission

RESPONSIBILITIES

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DEPED, TESDA and CHED

To make detailed descriptors for each qualification level based on learning standards in basic

education, competency standards of training regulations, and policies and standards of higher

education academic programs

PRC and CHED

To review the framework and contents of the licensure examinations of each of the professions

and align them with that of the PQF

DEVELOPMENT OF PQF

Issue: addressing job-skills mismatch

Participation of the Industry Sector

Industry sector representatives shall be consulted and tapped in detailing and application of the

PQF to ensure alignment of educational outcomes to job requirements

8-LEVEL QUALIFICATIONS DESCRIPTORS

Defined in terms of 3 domains

1. knowledge, skills and values (the kind of knowledge and skills involved)

2. application (the context in which the knowledge and skills are applied)

3. degree of independence (responsibility and accountability)

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LEVEL 1

KNOWLEDGE, SKILLS AND VALUES Knowledge and skills that are manual or concrete or

practical and/or operational in focus.

APPLICATION Applied in activities that are set in a limited range of

highly familiar and predictable contexts; involve

straightforward, routine issues which are addressed by

following set rules, guidelines or procedures.

DEGREE OF INDEPENDENCE In conditions where there is very close support, guidance

or supervision; minimum judgment or discretion is

needed.

QUALIFICATION TYPE NATIONAL CERTIFICATE I

LEVEL 2

KNOWLEDGE, SKILLS AND VALUES Knowledge and skills that are manual, practical and/or

operational in focus with a variety of options.

APPLICATION Applied in activities that are set in a range of familiar and predictable contexts; involve routine issues which

are identified and addressed by selecting from and following a number of set rules, guidelines or

procedures.

DEGREE OF INDEPENDENCE In conditions where there is substantial support,

guidance or supervision; limited judgment or discretion

is needed.

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QUALIFICATION TYPE NATIONAL CERTIFICATE II

LEVEL 3

KNOWLEDGE, SKILLS AND VALUES Knowledge and skills that are a balance of theoretical

and/or technical and practical.

Work involves understanding the work process,

contributing to problem solving, and making decisions to

determine the process, equipment and materials to be

used.

APPLICATION Applied in activities that are set in contexts with some unfamiliar or unpredictable aspects; involve routine and

non-routine issues which are identified and addressed by interpreting and/or applying established guidelines or

procedures with some variations.

DEGREE OF INDEPENDENCE Application at this level may involve individual

responsibility or autonomy, and/or may involve some

responsibility for others. Participation in teams including

team or group coordination may be involved.

QUALIFICATION TYPE NATIONAL CERTIFICATE III

LEVEL 4

KNOWLEDGE, SKILLS AND VALUES Knowledge and skills that are mainly theoretical and/or

abstract with significant depth in one or more areas;

contributing to technical solutions of a non-routine or

contingency nature; evaluation and analysis of current

practices and the development of new criteria and

procedures.

APPLICATION Applied in activities that are set in range of contexts,

most of which involve a number of unfamiliar and/or

unpredictable aspects; involve largely non-routine issues

which are addressed using guidelines or procedures

which require interpretation and/or adaptation.

DEGREE OF INDEPENDENCE Work involves some leadership and guidance when

organizing activities of self and others

QUALIFICATION TYPE NATIONAL CERTIFICATE IV

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LEVEL 5

KNOWLEDGE, SKILLS AND VALUES Knowledge and skills that are mainly theoretical and/or abstract with significant depth in some areas together

with wide-ranging, specialized technical, creative and conceptual skills. Perform work activities demonstrating breadth, depth

and complexity in the planning and initiation of alternative approaches to skills and knowledge applications across a broad range of technical and/or

management requirements, evaluation and coordination.

APPLICATION Applied in activities that are supervisory, complex and non-routine which require an extensive interpretation and/or adaptation/ innovation.

DEGREE OF INDEPENDENCE In conditions where there is broad guidance and

direction, where judgment is required in planning and selecting appropriate equipment, services and

techniques for self and others. Undertake work involving participation in the development of strategic initiatives, as well as personal

responsibility and autonomy in performing complex technical operations or organizing others

QUALIFICATION TYPE DIPLOMA

LEVEL 6

KNOWLEDGE, SKILLS AND VALUES Graduates at this level will have a broad and coherent knowledge and skills in their field of study for professional work and lifelong learning

APPLICATION Application in professional work in a broad range of

discipline and/or for further study

DEGREE OF INDEPENDENCE Independent and /or in teams of related field

QUALIFICATION TYPE Baccalaureate Degree

LEVEL 7

KNOWLEDGE, SKILLS AND VALUES Graduates at this level will have advanced knowledge

and skills in a specialized or multi-disciplinary field of study for professional practice, self-directed research and/or lifelong learning

APPLICATION Applied in professional work that requires leadership and

management in a specialized or multi-disciplinary professional work and/or research and/or for further

study

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DEGREE OF INDEPENDENCE Independent and or in teams of multidisciplinary

QUALIFICATION TYPE Post-Baccalaureate Program

LEVEL 8

KNOWLEDGE, SKILLS & VALUES Graduates at this level have highly advanced systematic

knowledge and skills in highly specialized and/or complex multidisciplinary field of learning for complex research and/or professional practice or for the

advancement of learning

APPLICATION Applied in highly specialized or complex multi-disciplinary field of professional work that requires innovation,

and/or leadership and management and/or research in a specialized or multi-disciplinary field

DEGREE OF INDEPENDENCE Independent and/or in teams of multi-disciplinary and more complex setting

QUALIFICATION TYPE Doctoral Degree and Post-Doctoral Programs

BENEFITS

For the Person

Encourages lifelong learning allowing the person to start at the level that suits him and

then build-up his qualifications as his needs and interests develop and change over time

Certificates and licenses are recognized by government

For the Employer

Assures that standards and qualifications are consistent to job requirements/demand

Provide common understanding on standards, qualifications and levels

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For the Education and Training Providers

Ensures transparency in training provision, conformance to standards and preciseness of

accountability for learning outcomes

Provides common understanding of policies and guidelines on credit transfer,

articulation, portability, bridges pathways and recognition of prior learning

For the Authorities

Provides the standards, taxonomy and typology of qualifications as bases for granting

approvals to providers and stakeholders

Harmonizes qualifications in education and training across Philippines

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Structure: Domains

1. Knowledge and Skills

2. Application

3. Responsibility

Dreyfus Model of Skill Acquisition

Craig McClure, MD

EOSG

University of Arizona

March 2005

Dreyfus Model of Competency Development

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ASSUMPTION: The model may be applied in the process of engaging RNs in PROGRESSIVE

COMPETENCY enhancement programs where “trained mentors” in nursing works to facilitate

assisting RNs go through the various levels of career progression until they reach the peak of

professional advancement as provided for in the policy framework.

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