9/16/2012

1

Blood pressure: Pathophysiology & Clinical

Management

Shahab Noori, MD

Associate Professor of Pediatrics

Division of Neonatology

September 20, 14:00 60 min

Insult Compensated

shock

Uncompensated

shock

Irreversible

shock

BP maintained Hypotension Multiorgan failure

Progression of Shock

Rationale for recognition and treatment of hypotension: a) Prevention of progression of shock to irreversible stage

b) Association with brain injury and poor developmental outcome

20

25

30

35

40

45

50

55

Me

an

BP

(m

m H

g)

0 12 24 36 48 60 72

27-32 weeks

33-36 weeks

37-43 weeks

23-26 weeks

1. Nuntnarumit et al, Clin Perinatol; 1999:26:981

* = 90% of neonates will have a mean BP value at or above the lower limit of the confidence interval

Lower Limit of the 80% Confidence Interval of BP in Neonates ( First 3 Postnatal Days)1

Gestational- and Postnatal-Age Dependence of BP

Age (h)

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Definition of Hypotension in the VLBW Neonate

Hypotension has been defined as1:

a) Mean BP (mmHg) < gestational age (wks)

b) Mean BP ≤5th (10th) percentile for gestational and

postnatal age

c) Mean BP < 28-30 mmHg

d) “Permissive Hypotension” with no defined value

1. Noori S. et al. Clin Perinatol 2009;36:723-36

Poiseuille’s Law:

Q = P x r4

8l

P1 P2

r

l

Q =

Ohm’s Law:

R

P Q = flow

P = pressure gradient

= 3.14

r = radius

= viscosity

l = length

R = resistance

Blood Flow vs. Blood Pressure

Q =

Ohm’s Law:

R

P

Blood Flow vs. Blood Pressure

Cardiac Output = Blood Pressure

Blood Pressure = Cardiac Output x Peripheral Vascular Resistance

Blood Pressure = x Peripheral Vascular Resistance x 2 Cardiac Output

2

Peripheral Vascular Resistance

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BP = CO x SVR

Systemic Blood Pressure

Dependent Variable

Systemic Resistance

Independent variable

(Vasopressors, Lusitropes)

Systemic Flow Independent variable

(Inotropes)

Non-vital organ blood flow distribution

O2 Delivery to

Meet O2 Demand

When OBF regulation exhausted:

1. Capillary recruitment 2. O2 extraction

Systemic blood flow affected by

1. Autonomic, endocrine, paracrine, autocrine regulators of cardiac function

2. GA, PNA, shunts (PDA, PFO) 3. pH, PaCO2, PaO2, electrolytes (Ca++

i) 3. Pathology: cytokines, chemokines

PRINCIPLES OF CARDIOVASCULAR PHYSIOLOGY: BLOOD PRESSURE, BLOOD FLOW, BLOOD FLOW DISTRIBUTION, VASCULAR RESISTANCE

Resistance affected by:

1. Autonomic, endocrine, paracrine, autocrine regulators of vascular function

2. GA, PNA, shunts, vascular anatomy 3. pH, PaCO2, PaO2, electrolytes (Ca++

i) 4. 3. Pathology: cytokines, chemokines

Vital organ blood flow distribution (brain, heart,

adrenals)

Soleymani et al, J Perinatol 2010; 30:S38-S45

Adequacy of blood flow is the goal

but

cannot be ensured by clinical exam

(e.g. cap refill time) and laboratory test

(e.g. lactate)

Osborn DA et al. Arch Dis Child 2004;89:F168-73

Miletin J et al. Eur J Pediatr. 2009;168:809-13

de Boode WP. Early Hum. Dev. 2010; 86:137–141

Vast majority of studies show an

association between hypotension and

brain injury/outcome

What is the cause of poor outcome?

Hypotension

Treatment

Hypotension+treatment

Other (hypotension is a marker)

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Indicators of Hypotension during first 24 hrs and Neurodevelopmental Outcome at 24 months in Preterm Infants < 28 GA

1) Logan J W et al. Arch Dis Child 2011; 96:F321-8

After adjusting for confounders, none of the indicators of hypotension were associated with: 1) an MDI <70 or a PDI <70 2) Indicators of white matter damage or cerebral palsy

2) Logan J W et al. J Perinatol. 2011; 31:524-34

(n=945)

Challenges in Assessing Effect of Hypotension on Outcome

• Common practice of treating hypotension

• Temporal relation to other factors affecting organ perfusion (e.g. PDA)

• Dysregulated inflammation

• Lack of definition of hypotension based on vital organ blood flow

• Lack of RCT evaluating the effect of hypotension and treatment on outcome

Batton BJ et al. J Pediatr 2012; 161:65-9

Feasibility Study of Early Blood Pressure Management in Extremely Preterm Infants

• In seven NICUs and among a population of 336 only 10 were studied in 1 year! • Consent obtained in 17% of eligible infants. • All neonates with pre-eligible consents (prenatal and postnatal) were not enrolled.

Attending refused (n=13)

Of 48 not enrolled, 41 (85%) received treatment for hypotension

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Factors Affecting the Potential Impact

of Hypotension on Outcome

Duration 1-3

Loss of autoregulation 4,5

Hypercarbia 6,7

Hypoxia 2

Metabolic acidosis 3

1. Hunt et al. J Pediatr. 2004;145:588-92

2. Low JA et al. Acta Paediatr 1993;82:433-7

3. Goldstein RF et al. Pediatrics 1995;95:238-43

4. O’ Leary H. Pediatrics 2009;124:302-9

5. Wong FY et al. PLoS one 2012;7:e43165

6. Kaiser et al, Pediatr Res 2005; 58:931

7. Noori et al. APS-SPR 2011

Outcome

Average MBP

Death and any

disability

Death

Abnormal

motor

*OR (95% CI) adjusted for gestation, use of postnatal

steroids, and level of maternal education

0.84 (0.52–1.34)

0.98 (0.43–2.26)

1.18 (0.51–2.73)

First 12 h

Abnormal DQ 0.86 (0.52–1.44)

Hunt et al. J Pediatr. 2004;145:588-92

0.68 (0.42–1.09)

0.49 (0.26–0.93)

1.01 (0.48–2.10)

0.79 (0.47–1.31)

1.25 (1.03–1.51)

1.46 (1.15–1.84)

0.98 (0.74–1.30)

1.15 (0.93–1.43)

1.48 (1.07–2.04)

1.47 (1.06–2.04)

1.17 (0.77–1.77)

1.48 (1.01–2.16)

First 24 h

% Readings MBP < GA

First 12 h First 24 h

Hypotension (Mean BP < GA) and Neurodevelopmental

Outcome at 3 years

n=126

Case 1

• A set of twin were born at 26 3/7 week via c-sec with no premature rupture of membrane. Apgar scores were 71 and 85. Both received surfactant and were put on conventional mechanical ventilation. Blood pressure and capillary refill were normal in the first week.

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0

20

40

60

80

100

0 4 8 12 16 20 24 28 32 36 40 44 48 52 56 60 64 68 72

rSO2 SPO2 Extraction

0

20

40

60

80

100

0 4 8 12 16 20 24 28 32 36 40 44 48 52 56 60 64 68 72

rSO2 SPO2 Extraction

0

20

40

60

80

100

0 4 8 12 16 20 24 28 32 36 40 44 48 52 56 60 64 68 72

rSO2 SPO2 Extraction

Twin

A

0

20

40

60

80

100

0 4 8 12 16 20 24 28 32 36 40 44 48 52 56 60 64 68 72

rSO2 SPO2 Extraction

Twin

B

* * * * *

* * *

*

*

Normal HUS: Normal Normal Normal Normal Normal Normal

Normal HUS: Normal Normal G1 IVH G4 IVH

(hours)

(hours)

(%)

(%)

MCA mean velocity

(cm

/s)

(cm

/s)

0

10

20

30

40

50

60

70

80

90

1 3 5 7 9 11 13 15 17 19 21 23 25 27 29 31 33 35 37 39 41 43 45 47 49 51 53 55 57 59 61 63 65 67 69 71 73 75

Twin A Twin B

Hours After Birth

Pa

CO

2 (

mm

Hg

)

Positive linear relationship between PaCO2 and MCA-MV

(R2=0.3, p<0.0001).

Relationship between Middle Cerebral Artery Mean

Velocity (MCA-MV) and PaCO2

(First 3 Days after Birth, GA 25.9 ± 1.4 wks, hemodynamically stable)

0

5

10

15

20

25

30

35

40

45

20 30 40 50 60 70 80

MC

A-M

V (

cm/s

)

PaCO2 (mmHg)

n= 78 data pairs in 21 subjects

Noori et al. APS-SPR 2011 (unpublished)

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• Using piece-wise bilinear regression models, a breakpoint was identified at 51-53 mmHg of PaCO2.

• Significant increase in CBF with CO2 above low 50’s

Relationship between MCA-MV and PaCO2 in First 3 Postnatal Days

0

5

10

15

20

25

30

35

40

45

20 30 40 50 60 70 80

MC

A-M

V (

cm/s

)

PaCO2 (mmHg)

Noori et al. APS-SPR 2011 (unpublished)

R2=0.49, p <0.0001

n= 78 data pairs in 21 subjects

A slope of near or equal to 0 suggest intact cerebral autoregulation

Slope of autoregulatory plateau

CBF-MABP relationship in the neonate

Effect of Hypercapnia on Cerebral Blood Flow Autoregulation in

43 Ventilated VLBW Neonates

Kaiser et al, Pediatr Res 2005; 58:931

CBF autoregulation is affected by PaCO2

CBF and BP relationship adjusted for CO2 level

• MCA-MV had positive linear relationship with BP when adjusted for CO2

• No relationship when CO2 < 51 mmHg

• A trend for positive linear relationship when CO2 ≥ 51 mmHg

• Attenuation of CBF autoregulation with high CO2

0

10

20

30

40

50

60

70

10 15 20 25 30 35 40 45 50

MC

A-M

V (

cm/s

)

MBP (mmHg)

PaCO2 < 51 mmHg

0

10

20

30

40

50

60

70

10 15 20 25 30 35 40 45 50

MC

A-M

V (

cm/s

)

MBP (mmHg)

PaCO2 ≥ 51 mmHg R2 = 0.007

P = 0.5

R2 = 0.133

P = 0.09

Noori et al. APS-SPR 2011 (unpublished)

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Hypotension in Extremely Preterm Infants: Summary

• Hypotension is associated with poor outcome

• Adequacy of organ blood flow is the most important parameter but cannot be verified by clinical exam and laboratory tests

• “Hypotension” should be considered as one of the screening tool for adequacy of CV function

• Duration of hypotension, impairment of autoregulation and presence of co-existing derangements (hypoxemia, extremes of CO2, hsPDA, metabolic acidosis) may augment the adverse effect of hypotension

Principles of CVS Supportive Care

• Target the underlying pathophysiology

• Choose the “right” medication

• Titrate the medication to the desired effect

• Take into account the developmentally regulated

differences in CVS in neonates versus older

children

• Consider down-regulation of adrenergic

receptors

• Beware of overshooting

Pathophysiology of Shock

Blood Pressure ∝ Cardiac output x Systemic Vascular Resistance

Neuroendocrine and

paracrin regulatory

mechanisms

Heart Rate x Stroke Volume

Afterload Preload Contractility

Arrhythmia

Hypovolemia

Diastolic dysfunction

Volume overload

Poor contractility

Hyperdynamic myocardium

High afterload

Low afterload

Vasodilation

Vasoconstriction

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Adrenergic, Dopaminergic and Vasopressin Receptors

Vascular Vascular Cardiac Cardiac Vascular/Cardiac Vascular

0

++++

0

0

0

0

0

++

0

0

0

0

++++

++++

++++

0

++++*

+/++

0

0

++++

0

0

0

0

Vasoconstriction

Vasodilation

+ Inotropy

+ Chronotropy

Cond. Velocity

++++

0

0

0

0

α1 / α 2 β 2 α 1 β 1 / β 2 DA1 / DA2 V1a

Selecting the “right” medication:

Cardiovascular actions of adrenergic receptors

* = renal, mesenteric, coronary circulation > pulmonary circulation > extracranial vessels of the neck

Noori & Seri. Clin Perinatol 2012; 39:221-38.

Selecting the “right” medication:

Mechanisms of action of vasopressors, inotropes, and lusitropes

Adrenergic, Dopaminergic and Vasopressin Receptors

0

0/+

++

++

++

+++

0

0

0

+

++

++

++

++

+++

0

0

0

0

++++

++++

+++

++++

++++

0

0

0

0

0

0

++++

0

0

0

0

0

0

0

0

0

0

0

++++

0

0

Phenylephrine

Norepinephrine

Epinephrine

Dopamine

Dobutamine

Isoprenaline

Vasopressin

PDE-III Inhibitors

PDE-V Inhibitors

++++

++++

++++

++++

+/0

0

0

0

0

Vascular Vascular Cardiac Cardiac Vascular/Cardiac Vascular

α1 / α 2 β 2 α 1 β 1 / β 2 DA1 / DA2 V1a

Noori & Seri. Clin Perinatol 2012; 39:221-38.

Mean BP (mmHg)

CB

F (

ml/

10

0g

/min

)

Mean BP (mmHg)

n=17 preterm infants

Control

Pre-Dopamine Dopamine

Munro MJ. et al. Pediatrics 2004;114:1591

Avoid Excessive increase in BP

• CBF may be low in hypotensive preterm infants

• Once on vasopressor (e.g. dopamine), CBF improves BUT because of

presence of a direct correlation with blood pressure (loss of autoregulation) →

reperfusion brain injury ?

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Pathophysiology of Shock

Blood Pressure ∝ Cardiac output x Systemic Vascular Resistance

Neuroendocrine and

paracrin regulatory

mechanisms

Heart Rate x Stroke Volume

Afterload Preload Contractility

Arrhythmia

Hypovolemia

Diastolic dysfunction

Volume overload

Poor contractility

Hyperdynamic myocardium

High afterload

Low afterload

Vasodilation

Vasoconstriction

Cardiovascular

Compromise

Vasodilation

- Septic shock

- Systemic inflammatory

disease, (e.g. NEC)

- Pressor-resistant

hypotension

de Waal K, Evans N. J Pediatr 2010;156:918-22

Preterm Infants with Sepsis Have High Cardiac Output and Low SVR

• No change in flow and mild increase in SVR among survivors

• Non-survivor had a significant drop in cardiac output and a

sharp rise in SVR

n=20 (5 died), GA 27 (25-32) weeks, clinical sepsis or NEC, 15 had positive blood culture

* *

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SVRI And Cardiac Index (CI) In 30 Children with Fluid-resistant Septic Shock

Brierley J. et al. Pediatrics 2008;122:752-759

Central venous catheter-related

Community acquired

High CI > 5.5

• Hemodynamic response may vary depending on the bacteria

• Septic shock in late stages may be associated with myocardial

dysfunction

Vasodilatory Shock

• Treatment

– Volume

– Vasopressor (e.g. dopamine, epinephrine)

– Corticosteroid as a second line

*Significant hemodynamic variability among preterm infants who survive1

1. de Waal K et al. J Pediatr 2010

Cardiovascular

Compromise

Vasodilation

- Septic shock

- Systemic inflammatory

disease, (e.g. NEC)

- Pressor-resistant

hypotension

Poor Contractility

- Asphyxia

- Perinatal depression

- Septic shock (late stage)

- Dilated cardiomyopathy

- LV non-compaction

- Maladaptation after birth

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Case #2

• A preterm infant was born at 24 1/7 week (BW 805g) via vaginal delivery after prolonged rupture of membrane without signs of chorioamnionitis. Apgar scores were 21, 15, 210 and the baby required a brief chest compression. Initial ABG 7.05/92/102/-5/25 on SIMV FiO2 0.35. Switched to HFO with normal blood gases afterward.

• At 12 hrs

– ABG 7.33/37/47/-6/20 - BP 31/25 28

– CRT <2 sec - Hct 47

RVO (ml/k/min) 49 228

M-m

ode (L

V)

Short a

xis

vie

w (L

V)

Pulm

. Dop

ple

r

septum

post Wall

LV

SF 22% SF 37%

RVO (ml/k/min)

Pulm. Artery (systemic flow) Middle Cerebral Artery

A 4 hours old 25 6/7 wk preterm infants with severe

myocardial dysfunction, low systemic and cerebral blood flow

due placental abruption. Patients responds to dobutamine….

Dobutamine started Dobutamine started

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Robel-Tillig et al. Early Hum Dev. 2007;83:307

Cardiovascular Impact of Dobutamine in Neonates with Myocardial Dysfunction

Card

iac O

utp

ut

(ml/k/m

in)

SM

A –

SV

(cm

/s)

Ren

al

a. – S

V (

cm

/s)

A.

Cere

bra

l a. – S

V (

cm

/s)

Pre Dob 20 min Dob 8-10h

Pre Dob 20 min Dob 8-10h Pre Dob 20 min Dob 8-10h

Pre Dob 20 min Dob 8-10h

*

*

*

*

n=20, GA 29.4 4.4 wk, postnatal age 2 2.1 days, dobutamine 9.1 1.1 mcg/k/min

Asphyxia/Perinatal Depression

• Cause of circulatory compromise

– myocardial dysfunction (± compensatory

vasoconstriction)

• Treatment

– inotropes e.g. dobutamine

– avoid excessive fluid boluses

Cardiovascular

Compromise

Vasodilation

- Septic shock

- Systemic inflammatory

disease, (e.g. NEC)

- Pressor-resistant

hypotension

Poor Contractility

- Asphyxia

- Perinatal depression

- Septic shock (late stage)

- Dilated cardiomyopathy

- LV non-compaction

- Maladaptation after birth

High Afterload

- Maladaptation after birth

- Dilated cardiomyopathy

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Adapted from Rowland & Gutgesell, Am J Cardiol 1995

Sensitivity of Immature Myocardium to Afterload

Contr

actilit

y

Afterload

Treatment

Inotrope (e.g. dobutamine)?

Lucitrope (e.g. milrinone)?

Cardiovascular

Compromise

Vasodilation

- Septic shock

- Systemic inflammatory

disease, (e.g. NEC)

- Pressor-resistant

hypotension

High Afterload

- Maladaptation after birth

- Dilated cardiomyopathy

Hypovolemia

- Acute blood loss

- Umbilical cord avulsion

- Subgaleal hemorrhage

- insensible water loss

- Polyuria

Poor Contractility

- Asphyxia

- Perinatal depression

- Septic shock (late stage)

- Dilated cardiomyopathy

- LV non-compaction

- Maladaptation after birth

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Hemodynamic Effects of Delayed Cord Clamping in

Premature Infants

Sommers et al. Pediatrics. 2012; 129:e667-72

RCT, n=41, mean GA ~28 weeks, DCC=45 s, ICC= 5 s

• Higher SVC flow in delayed cord clamping group

• Higher RVO in delayed cord clamping group only at 48 hours

• No difference in MCA or SMA flow velocity, shortening fraction

Post Abdominal Surgery

1 month old former 23 week premie with NEC and perforation. Post-operative: Received multiple fluid boluses and escalating dose of dopamine up to 25 mcg/kg/min for persistent hypotension & metabolic acidosis BP 26/17 21 Base excess -12.8 Echo SF 48% LVO 243 ml/kg/min

Case #3

Cardiovascular

Compromise

Vasodilation

- Septic shock

- Systemic inflammatory

disease, (e.g. NEC)

- Pressor-resistant

hypotension

Diastolic Dysfunction

- Tension pneumothorax

- Cardiac tamponade

- Hypertrophic

cardiomyopathy

(e.g. IDM)

High Afterload

- Maladaptation after birth

- Dilated cardiomyopathy

Hypovolemia

- Acute blood loss

- Umbilical cord avulsion

- Subgaleal hemorrhage

- insensible water loss

- Polyuria

Poor Contractility

- Asphyxia

- Perinatal depression

- Septic shock (late stage)

- Dilated cardiomyopathy

- LV non-compaction

- Maladaptation after birth

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Case #4

• A 5.4 kg term infant, born to an insulin-dependent diabetic mother, presents with hypotension and moderate metabolic acidosis 2 hours after birth. Echocardiogram shows significant myocardial hypertrophy, dynamic left ventricular outflow tract obstruction, a closing PDA with bidirectional shunting and otherwise normal cardiac anatomy.

Normal IDM with HCM

Septum

Post Wall

Echocardiogram: M-mode

LV LV

Hypertrophic Cardiomyopathy

• Cause of circulatory failure

– diastolic dysfunction

• low preload

• hyperdynamic myocardium

– dynamic LV outflow obstruction

• Treatment

– VOLUME

– Beta-blocker (esmolol drip)

– Vasopressor

– AVOID inotropes

Cardiovascular

Compromise

Vasodilation

- Septic shock

- Systemic inflammatory

disease, (e.g. NEC)

- Pressor-resistant

hypotension

Diastolic Dysfunction

- Tension pneumothorax

- Cardiac tamponade

- Hypertrophic

cardiomyopathy

(e.g. IDM)

Shunt

- PDA

- AV malformation

High Afterload

- Maladaptation after birth

- Dilated cardiomyopathy

Hypovolemia

- Acute blood loss

- Umbilical cord avulsion

- Subgaleal hemorrhage

- insensible water loss

- Polyuria

Poor Contractility

- Asphyxia

- Perinatal depression

- Septic shock (late stage)

- Dilated cardiomyopathy

- LV non-compaction

- Maladaptation after birth

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Case # 5

• A preterm infant (twin A) was born at 31 1/7 weeks gestation (BW 1180g, 8%ile) via c-sec due to abnormal cord Doppler study. No signs of chorioamnionitis. Apgar scores were 41 and 75. The baby is on no respiratory support and blood gases are normal. However, the baby has been hypotensive despite receiving a bolus of NS. Now at 3 hours after birth, blood pressure is 34/14 (21) and capillary refill is 2-3 sec.

1) No intervention; continue close monitoring

2) Give another 10-20 ml/kg 0.9 NS bolus

3) Start dobutamine at 5 mcg/kg/min and titrate

4) Start dopamine at 5 mcg/kg/min and titrate

5) Start epinephrine at 0.05 mcg/kg/min and titrate

With regard to hemodynamic status, what would be the

best course of action:

SF 34%

LVO = 377 ml/k/min

M-mode (LV)

Short axis view (LV)

Aorta Doppler

Middle Cerebral Artery Doppler

MV 23 cm/s

15

20

25

30

35

40

3hr 9hr 33hr

MA

P (

mm

Hg)

-20

-10

0

10

20

30

40

50

60

70

80

3hr 9hr 33hr

LVO SVR MAP

% c

han

ge

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Not all “hypotensive” infant need

treatment if adequacy of organ blood

flow can be verified

Objective Assessment of Hemodynamics

Beyond BP

• Functional echocardiography

• Non-invasive continuous cardiac output

monitor

• Tissue oxygen saturation

– Near infra-red spectroscopy

– Visible light spectroscopy

Continuous Cardiac Output Monitor Based on Electrical Cardiometry

(Thoracic Electrical Biompedance)

Non-invasive

Simple to use

Need to be further validated

Aesculon ®

Aorta prior to Aortic

Valve Opening

Aorta after Aortic Valve

Opening

No Flow →

Random Orientation

Pulsatile Flow →

Alignment

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0

100

200

300

400

500

600

700

800

900

ᴏ

ᴏ ᴏ

Echo Electrical Cardiometry

LV

O (m

l/m

in)

Continuous Non-Invasive Cardiac Output Measurements in the

Neonate by Electrical Cardiometry:

A Comparison with Echocardiography

115 paired measurements in 20 healthy term neonates in first 2 days

Noori et al. Arch Dis Child 2012; 97:F340-3

Agreement between Left Ventricle Output Estimated by Echocardiography

and Electrical Cardiometry.

Noori et al. Arch Dis Child 2012; 97:F340-3

True precision = 31% which is considered clinically acceptable

115 paired measurements in 20 healthy term neonates in first 2 days

Bias 153 ± 56 ml/min

Limit of agreement = 43, 267 ml/min

NICOM consistently under-read LVO by 31 ± 8.8% (Limit of agreement = 15%, 46%)

Weisz et alNeonatology. 2012; 102:61-7

Non-invasive Cardiac Output Monitoring In Neonates Using Bioreactance:

A Comparison With Echocardiography

(ml/

min

)

97 paired measurements in 10 neonates 31-41 weeks gestation

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Fore-Sight ®

INVOS®

INVOS®

Tissue Oxygen Saturation: Near Infra-Red

Spectroscopy

Tissue Oxygen Saturation: Visible Light Spectroscopy

(T-Stat, SPECTROS)

Buccal tissue saturation is 61 to 72% in normal term neonates Correlates with LVO May be useful in detecting early stage of shock

Noori et al. J Perinatol 2011

BP or clinical assessment of flow

BP + clinical assessment of flow

+ pathophysiology

Identify underlying

pathophysiology

+

Echocardiography

+

Organ blood flow

Ensuring adequate

organ blood flow and

function

Identify possible

underlying

pathophysiology based

on the history

Level of Monitoring