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1
Q

Persistent Pulmonary Hypertension of the Newborn Definition

A

PPHN is persistence after birth of the high pulmonary arterial pressure (PPA), often suprasystemic, that is characteristic of the fetal circulation.

PPHN may occur with or without apparent pulmonary disease

2
Q

Persistent Pulmonary Hypertension of the Newborn Pathology

A

In fetal life, pulmonary blood flow (Qp) is low (5-10% of cardiac output [CO]) due to high pulmonary vascular resistance (PVR) and shunts (i.e., foramen ovale, ductus arteriosus) which permit blood to bypass the pulmonary vascular bed. At birth, PVR normally falls dramatically (due to lung inflation and oxygenation), Qp increases to 100% of CO and, by 24 hours after birth, PPA has fallen to about 50% of systemic arterial pressure.

When this normal transition fails, PVR and PPA remain elevated, Qp stays low, right to left shunting occurs at the foramen ovale and ductus arteriosus, and hypoxemia results. Several factors influence PVR; among these, acidosis and alveolar hypoxia are potent pulmonary vasoconstrictors.

3
Q

Clinical Causes of PPHN

A

Abnormal pulmonary vascular development (e.g., increased pulmonary vascular smooth muscle due to chronic fetal hypoxia, maternal diabetes, alveolar capillary dysplasia)

  • Pulmonary hypoplasia with associated hypoplasia of pulmonary vasculature (e.g., congenital diaphragmatic hernia, Potter’s syndrome, prolonged oligohydramnios)
  • Postnatal elevation in pulmonary vasoconstrictors (e.g., sepsis, pneumonia, aspiration syndromes, perinatal asphyxia)
  • Congenital heart disease (e.g., total anomalous pulmonary venous return with obstruction).
4
Q

Treatment of PPHN

A

Primary treatment is supplemental oxygen with high inspired oxygen concentrations- Start with 100% O2. Maintain pre-ductal PaO2at 90 to 100 mmHg.

Correct metabolic acidosis (NaHCO3, THAM).

Correct respiratory acidosis with assisted ventilation.

Inhaled nitric oxide (iNO): dose is 20 ppm

Adequate sedation, pharmacologic paralysis, as needed. Minimize handling

ECMO

5
Q

Compare and describe the indications for mechanical ventilation for adult, pediatric and neonatal patients

A

All patient populations have the following indications: apnea, acute ventilatory failure, impending ventilatory failure and severe refractory hypoxemia.

The neonatal population also adds surfactant therapy and congenital defects/abnormalities as indications.

The differences are in the specific criteria required to meet the indication.

6
Q

Acute ventilatory failure:

A

Adults/Peds: PaCO2> 55 mmHg with a pH < 7.25

Neonates: pH of < 7.25 despite the use of CPAP with supplemental oxygen of FiO2> 0.60

7
Q

Impending ventilatory failure

Adults

A

Tachypnea, dyspnea, accessory muscle use, tracheal tug, pursed lip breathing etc.

May use objective measures (MIP, VC, Vt, Vd/Vt etc) to help quantify our findings.

Remember all of these things may not be done clinically and multiple factors are assessed (e.g. may measure MIPS on a neuromuscular patient but not do a Vd/Vt measurement)

8
Q

Impending ventilatory failure

Ped

A

Young peds you will see similar signs and symptoms to the neonate, may include head bobbing

Older peds-more similar to adults

9
Q

Impending ventilatory failure

Neo

A

retractions, expiratory grunting, nasal flaring, tachypnea, increasing oxygen requirements etc…

Non-invasive may be trialled if pH > 7.25

10
Q

Severe refractory hypoxemia

A

Adults: use PF ratios (< 200 critical), A-a gradient (>350 critical), and PaO2/PAO2(<0.15 critical) to help define

Neonates: use guideline of a PaO2< 50 mmHg despite use of CPAP and supplemental oxygen (with FIO2≥0.6)

11
Q

Ti dyn calculation on VC

A

TiDyn= VT/Flow (lps)

12
Q

What are the normal goal ranges for ABGs in an adult patient?

A

Normal blood gas values for ventilation (pH 7.35-7.45, PaCO235-45 mmHg)

PaO260-100 mmHg (Note: remember this depends on what the patient’s underlying condition is, if they have normal lungs a higher PaO2would be desirable and expected, if they have a head injury would want to see PaO2’s in the 80-120 mmHg range.

Saturations³90% (see note above)

13
Q

ABG Goals for ELBW (<28 week)

A

pH ≥7.25

PaCO2 45-65

PaO2 50-70

SaO2 85-92

14
Q

ABG Goals for ELBW (<28 week)

A

pH ≥7.25

PaCO2 45-55

PaO2 45-65

SaO2 85-92

15
Q

Lung Protective Strategies in Neo

A

pH ≥7.25 but use VT of ~ 4 mL/kg.

PaCO2is targeted at 45-55 mmHg initially.

PEEP is set to maintain recruitment but recruitment maneuvers are not used.

For Neonates PIPs are kept to < 25-30 cmH2O.

16
Q

Lung Protective Strategies in Adults

A

pH ≥7.25 and goal VTin the 6-8 mL/kg range (potentially as low as 4 mL/kg depending on Pplat).

PaCO2 is allowed to rise slowly.

PEEP is set to maintain recruitment and recruitment maneuvers may be used.

Pplat generally kept < 30 cmH2O

17
Q

Describe how auto-PEEP can interfere with patient-ventilator synchrony.

A

To trigger the ventilator a patient either has to inspire a certain set flow (for flow triggering) or cause a pressure drop below baseline in the circuit. When a patient has autoPEEP this creates an increased WOB as they must overcome the autoPEEP in their chest.

Eg. If pressure trigger set to -2 cmH2O, PEEP at 5 and autoPEEP is 10 cmH2O (and total PEEP is 15). The patient must reduce the circuit pressure to 3 cmH2O in order to trigger the ventilator meaning their inspiratory effort must reduce intrathoracic pressures from 15 cmH2O to at 3 cmH2O in order to trigger the vent.

Eg. If the flow trigger is set to 2 LPM, PEEP at 5 and autoPEEP is 10 cmH2O (and total PEEP is 15). The patient must still reduce intrathoracic pressure to less than 5 cmH2O in order to get a pressure gradient that results in flow into the patient and trigger the vent.

18
Q

Describe the theory behind lung recruitment maneuvers.

A

Done primarily in the adult patient population

One technique to achieve “open lung ventilation”

Use high CPAP pressures for 30s to 60s (to 120 s in sustained maneuvers) unstable alveoli and alveoli with long time constants are recruited, opening the lung up.

After recruitment return patient to their conventional settings, if PEEP is set appropriately (to stabilize the newly recruited lung units), it will result in better V/Q matching and reduced risk of VILI (ventilator-induced lung injury).

Can also do recruitment maneuvers on patients who are spontaneously breathing that are at risk of atelectasis, pneumonia etc. (e.g. patients with neuromuscular diseases like ALS, MD or spinal cord injury)

19
Q

What are the indications for lung recruitment maneuvers?

A

Atelectasis

CXR showing evidence of ALI/ARDS (diffuse bilateral infiltrates)

Increased oxygen index (OI), Calgary uses an OI of > 12

Patients requiring a high PEEP level

Patients who desat after a disconnection from the ventilator may be a candidate.

Body mass index > 30 as the extra weight in the abdominal area can predispose the patient to atelectasis

20
Q

What are the contraindications for lung recruitment maneuvers?

A

Pulmonary air leak syndromes

Recent, or active pneumo, or PIE

Bronchopleural fistula

Obstructive pulmonary disorder

Acute head injury

Hemodynamic instability

Pregnancy

21
Q

Describe why the SPO2 targets for a COPD patient are 88-92%.

A

Fear of oxygen-induced hypercapnia.

Theories behind this phenomenon include

Worsening of V/Q matching due to oxygen administration

Haldane effect

Hypoxic drive (of course the existence of hypoxic drive is controversial).

22
Q

Auto PEEP in COPD

A

Auto-PEEP is created due to dynamic hyperinflation

Forced exhalation causes airway closure due to the equal-pressure point moving distally in the airway

Most commonly seen in COPDers with a large emphysematous component

Increased resistance is primarily on exhalation – why “matching” PEEP to auto-PEEP can decrease WOB in a COPD patient

Adding extrinsic PEEP causes the airways to stay open on exhalation allowing for greater emptying of the lungs and decreasing auto-PEEP

23
Q

Auto PEEP in Asthma

A

Auto-PEEP created is due to high airway resistance resulting from bronchoconstriction, secretions and mucosal edema

Creates resistance to inspiration as well as expiration due to direct airway narrowing – fixed obstruction

More time is needed for exhalation

When combined with tachypnea seen in acute asthmatics and air-trapping, hyperinflation and autoPEEP result

Matching PEEP to autoPEEP in an asthmatic does not alleviate WOB it only increases total PEEP

24
Q

Compare the strategies used when ventilating an acute asthmatic patient versus an acute COPD patient.

A

Both focus on reducing autoPEEP by maximizing expiratory times (low RR, short TI).

PEEP is used to offset the autoPEEP in COPD but not in asthma.

Permissive hypercapnia is more likely to be used in asthma

PaCO2 targets in COPD are the patient’s normal values

Ventilator dependence is more of a concern in COPD therefore the time on FVS should be minimized (after an initial rest period and remember the patient could be rested on PS, it the PS level is high enough to give VTof 8 -10 mL/kg and patient has intact respiratory drive.

25
Q

Describe the strategy used when ventilating a neonate with HMD.

A
  • Surfactant therapy:
    • Neonate may be intubated for surfactant therapy and ventilated until stable, then extubated to CPAP
  • Lung protective strategy
    • Use smaller tidal volumes ( ~ 4 mL/kg) with a goal pH ≥7.25, and PaCO2 of 45-55 mmHg
    • Start on APV with 4 mL/kg target, may change to PC if leak present
    • PEEP should be set to maintain recruitment, generally use 6 cmH2O to start
    • Peak pressures are kept to < 25 cmH2O
    • HFO being considered if pressures are high, of if PEEP is ≥8 cmH2O
    • This approach is used for ventilation of neonates ≤32 weeks
26
Q

Describe the strategy when ventilating a neonate with PPHN.

A

Focus on reducing pulmonary vascular resistance

ABG goals are: pH 7.40-7.45, PaCO2 35-40 and PaO2 > 100 mmHg, these targets promote vasodilation of the pulmonary vasculature (decreasing PVR) and closure of the ductus arteriosus

Nitric oxide may be used as it is a selective pulmonary vasodilator, may also use sildenafil (off-label use)

Conventional mechanical ventilation can be used but if high pressures are required then non-conventional forms may be considered (HFO, HFJV, ECMO)

Testing for PPHN – Pre-ductal-post-ductal PaO2comparison – looks for a difference of 20 mmHg. Pre-ductal Rt. Radial, post ductal – umbilical artery. If comparing SpO2a general rule of thumb is 15%, however, this depends on the portion of the Hb-O2dissociation curve the patient is on, therefore, if there is a discrepancy further investigation warranted, but would likely treat as PPHN.

27
Q

Describe the strategy used when ventilating a neonate with a cyanotic heart defect.

A

Focus on maintaining a patent ductus arteriosus

Target ABGs mimic in utero conditions: pH 7.40, PaCO2 in the 40s, PaO2 in the 40’s (sat’s 70-80%)

Hypoxic gas mixtures may be used to achieve the PaO2 desired (ie. FIO2 of < 0.21, typically 17-19%)

May use IV Prostin to maintain PDA

28
Q

Describe the strategy used when ventilating a neonate with meconium aspiration syndrome.

A

Possible surfactant therapy (decided case by case)

Lung protective strategy (VT = 4 mL/kg)

Additionally concerned about hyperinflation and the development of PPHN, therefore, generally use ABG targets for PPHN (7.35-7.40 and 35-40 for PaCO2and PaO2> 100 mmHg)

May use NO, HFO, HFJV or ECMO

29
Q

Describe the strategy used when ventilating an infant with CLD.

A

Focuses on minimizing the PPV and FIO2.

Permissive hypercapnia is used, target pH ≥ 7.25, VTof 4-6 mL/kg

APV often works well with these babies

FIO2is minimized with target SpO2being 85-88% up to 94%

Need to be cautious as there is concern that the lower SpO2 may cause hypoxic pulmonary vasoconstriction, polycythemia… which can result in cor pulmonale

30
Q

Describe the strategy used when ventilating an infant with PIE.

A

Focuses on a lung protective strategy to minimize the PPV

Low VT (~4 mL/kg), with permissive hypercapnia (pH ≥ 7.25)

Keeping pressures to < 25 cmH2O

May position the neonates with the worst lung down

Directs most of ventilation to good lung

Perfusion goes to poor lung, helping with healing of the damaged lung

Severe cases HFO, HFJV or selective intubation of the good side is considered

31
Q

Describe the strategy used when ventilating a patient with CF.

A

Goal is to use non-invasive ventilation first

If invasive ventilation is required:

allow adequate time for expiration (obstructive disorder) use low VT, low RR, short TI, and possibly permissive hypercapnia

Heated humidity due to the thickened secretions

May require nebulized antibiotics +/- mucolytics

32
Q

Respiratory Effect From PPV

A

V/Q mistmatching: ventilation goes to gravity independent areas and perfusion goes to gravity dependent areas=result means increased deadspace and increased intrapulmonary shunting

VILI: ventilator induced lung injury (Kacmarek page 740); barotrauma, volutrauma, atelectatrauma, shear stress and biotrauma.

Air-trapping/autoPEEP: results in increased risk of VILI, contributes to pt-ventilator dyssynchrony

Oxygen toxicity: FIO2> 0.60 associated with increased risk of toxicity

33
Q

Muscular Effect From PPV

A

risk of atrophy of respiratory muscles if WOB removed for extended periods

34
Q

Metabolism Effect From PPV

A

when WOB removed then O2 consumption and CO2 production decrease; also critically ill patients overall have an increased metabolic rate

35
Q

Liver Effect From PPV

A

poor liver function due to reduced CO and blood pooling 2°to increased CVP

36
Q

Renal Effect From PPV

A

reduced urine output, stimulation of Renin-angiotensin-aldosterone system, stimulation of ADH release

37
Q

Renal Effect From PPV

A

reduced urine output, stimulation of Renin-angiotensin-aldosterone system, stimulation of ADH release

38
Q

ICP and CPP Effect From PPV

A

CPP may decrease due to a lower MAP (2°to reduced CO)

ICP increases due to an increased CVP (which impedes venous return from the brain)…this further reduces CPP

39
Q

CVS Effect From PPV

A

reduced stroke volume 2°to reduced venous return…leading to reduced CO in a patient who is cardiovascularly compromised

Altered R and L ventricular function (ie. interventricular shift from R to L)

40
Q

Barotrauma

A

this type results in rupture of A/C membrane and extra-alveolar air. This is the most acute and severe form of VILI

41
Q

Volutrauma

A

results due to overdistension of alveoli resulting in a damaged A/C membrane (becomes leaky just like in ARDS)

42
Q

Atelectatrauma

A

caused by the cyclic recruitment-derecruitment of unstable alveoli throughout a respiratory cycle. Shear stress results on the alveolar wall between a collapsed alveoli and recruited alveoli.

43
Q

Biotrauma

A

The release of inflammatory mediators from the lungs due to atelectatrauma, and volutrauma. These mediators enter the systemic system and can result in multi-system organ failure

44
Q

Disadvantages of Auto-PEEP

A

Increased risk of developing VILI

Increased risk of over-distending the lung (passing the upper inflection point on inspiration)

May reduce patient-ventilator synchrony

45
Q

Advantages of Auto PEEP

A

Improves oxygenation status (just as adding extrinsic PEEP does)

Sometimes (eg. with APRV ventilation strategy) we try to create it to aid in oxygenation

46
Q

Describe the harmful effects of mechanical ventilation that are specific to the neonatal population.

A
  • CLD/BPD:
    • related to PPV, FIO2, intubation, duration of therapy, degree of pulmonary prematurity
  • ROP:
    • Associated with exposure to high PaO2and fluctuating PaO2 levels, not the sole cause
    • Wean FIO2 slowly and make changes in small increments when possible
  • Intracranial hemorrhage
    • Associated with PPV but not necessarily caused by PPV
  • Hypocarbia
    • Associated with periventricular leukomalacia \maintain the goal PaCO2, don’t overventilate when bagging
    • Also associated with Cerebral Palsy
47
Q

Describe the additional VILI that may occur in neonatal patients.

A

BPD-Related to PPV, FiO2, intubation, duration of therapy, degree of pulmonary prematurity

PIE-Seen less frequently now due to more lung protective strategies and better pt-ventilator synchrony