RT 230 PPP-Unit A and Unit B

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RT 230

Unit A-

Indication, Setup and Monitoring of CMV

I NDICATIONS FOR CMV

Apnea

Acute ventilatory failure: A PCO

2 of more than

50mmHg with a pH of less than 7.25

Impending acute ventilatory failure

Based on lab data and clinical findings indicating that pt is progressing towards ventilatory failure

Quick tip: acute hypercapnic failure ph drops 0.8 for every

10mm hg rise in co2 chronic hupercapnic ph drops 0.03 for every 10 mmhg rise in co2

Clinical problems often resulting in impending ventilatory failure

Pulmonary abnormalities

RDS=Respiratory Distress Syndrome

Pneumonia

Pulmonary emboli

Mechanical ability of lung to move air=muscle fatigue

Ventilatory muscle fatigue

Chest injury

Thoracic abnormalities=scoliosis, kyphoscoliosis

Neurologic disease=GB, MG

Pleural disease=pleurasy

Clinical evaluation

Vital signs: Pulse and BP increase

Ventilatory parameters

V

T decreases

RR increases

Accessory muscle use increases

Paradoxical breathing (abdomen out, rib cage in)

Retractions may be noted

Development of impending acute vent failure may demonstrate

Progressive muscle weakness in pt with Neurologic disease

Increasing fatigue

ABGs demonstrating a trend toward failure

9am10am 11am 12pm 1pm pH 7.58 7.53 7.46 7.38 7.35

PCO

2

HCO

3

PO

2

22

21

60

28

22

55

35

23

50

42

24

43

48

24

40

Non-responsive hypoxemia

PaO

2

less than 50% on an FIO greater than 50%

2

PEEP is indicated

REFRACTORY HYPOXEMIA

P HYSIOLOGIC E FFECTS OF P OSITIVE P RESSURE

V ENTILATION

Increased mean intrathoracic pressure

Decreased venous return

Thoracic pump is eliminated***

Pressure gradient of flow to right side of heart is decreased

Right ventricular filling is impaired

Give fluid

Decreased cardiac output

Caused by decreased venous return

Give drugs and fluid

Monitor I and O. Normal urine output 1000-1500 cc/24 hours

THORACIC PUMP

The "thoracic pump" is the thoracic cavity, the diaphragm, the lungs, and the heart.

The diaphragm moves down, pressure in the cavity decreases and venous blood rushes through the vena cava via the right heart into the lungs. Pulmonary blood vessels expand dramatically, filling with blood, air and blood meeting across the very thin alveolar surface.

The deeper the inhalation, the more negative the pressure, the more blood flows, and the fuller the lungs become.

THORACIC PUMP

As the diaphragm moves up the pressure in the thoracic cavity reverses. Pulmonary blood vessels shrink ejecting an equal volume of blood out of the pulmonary veins into the left heart. The left heart raises the pressure and checks and regulates the flow. The more complete the

exhalation

, the more positive the pressure becomes and the more blood is ejected from the lungs.

Decrease exhalation, more pressure in cavity decrease CO

E FFECTS OF PPV CONT .

Increased intracranial pressure

Blood pools in periphery and cranium because of decreased venous return

Increased volume of blood in cranium increases intracranial pressure

Decreased urinary output

PPV could cause 30-50% decrease renal output

Decreased CO results in decreased renal blood flow

Alters filtration pressures and diminishes urine formation

Decreased venous return and decreased atrial pressure are interpreted as a decrease in overall blood volume

ADH is increased and urine formation is decreased

ADH=VASOPRESSIN

Roughly 60% of the mass of the body is water, and despite wide variation in the amount of water taken in each day, body water content remains incredibly stable. Such precise control of body water and solute concentrations is a function of several hormones acting on both the kidneys and vascular system, but there is no doubt that antidiuretic hormone is a key player in this process.

Antidiuretic hormone, also known commonly as arginine vasopressin

The single most important effect of antidiuretic hormone is to conserve body water by reducing the loss of water in urine. A diuretic is an agent that increases the rate of urine formation.

high concentrations of antidiuretic hormone cause widespread constriction of arterioles, which leads to increased arterial pressure.

Retention of fluids will cause EDEMA

E FFECTS OF PPV CONT .

Decreased work of breathing

Force to ventilate is provided by the ventilator

Increased deadspace ventilation

Positive pressure distends conducting airways & inhibits venous return

The portion of V

T that is deadspace increases

Greater percentage of ventilation goes to apices

Increased intrapulmonary shunt

Ventilation to gravity dependent areas is decreased

Perfusion to gravity dependent areas increase

Shunt fraction increases from 2-5% to 10%

A pulmonary shunt is a physiological condition which results when the alveoli of the lung are perfused with blood as normal, but ventilation (the supply of air) fails to supply the perfused region. In other words, the ventilation/perfusion ratio (the ratio of air reaching the alveoli to blood perfusing them) is zero. A pulmonary shunt often occurs when the alveoli fill with fluid, causing parts of the lung to be unventilated although they are still perfused

.

Intrapulmonary shunting is the main cause of hypoxemia (inadequate blood oxygen) in pulmonary edema and conditions such as pneumonia in which the lungs become consolidated.

The shunt fraction is the percentage of blood put out by the heart that is not completely oxygenated. A small degree of shunt is normal and may be described as 'physiological shunt'. In a normal healthy person, the physiological shunt is rarely over 4%; in pathological conditions such as pulmonary contusion , the shunt fraction is significantly greater and even breathing 100% oxygen does not fully oxygenate the blood.

[1]

E FFECTS OF PPV CONT .

Respiratory rate, V

T

, Inspiratory time, and flow rate can be controlled

May cause stress ulcers and bleeding in GI tract

C OMPLICATIONS OF M ECHANICAL

V ENTILATION

Complications related to pressure

Ventilator-associated lung injury (VALI)

High pressures are associated with barotrauma

Pneumothorax, pneumomediastinum, pneumopericardium, subcutaneous emphysema

Pneumothorax has decreased chest movement, hyperresonance to percussion, on affected side

If tension pneumothorax: medical emergency

Relieved by needle insertion, then chest tube

Use 100% oxygen to speed reabsorption.

Placing patient on CMV

Establish airway

Select V

T

8-12ml/kg of ideal body weight

Select mode - a/c sensitivity at minimal to not self cycle

Set pressure limit 10cmH

2

O above delivery pressure

Set sigh volume 1-1/2 to 2 times V

T

Sigh pressure 10cmH

2

O above sigh delivery pressure

Rate as ordered

PEEP as ordered: exp. resist, insp. hold, etc.

Set spirometer 100 cc less than patient volume

 check for function (turn on)

Modes

Control

All of WOB is taken over by ventilator

Sedation is required

Control mode is useful

During ARDS, especially if high PEEP is required or inverse

I:E ratio

Assist

Patient is able to control ventilatory rate

Should not be used for continuous mechanical ventilation if pt is apneic

Assist/control

Pt able to control vent rate as long as spontaneous rate > backup rate

Machine performs majority of WOB

Sedation is often required to prevent hyperventilation

Is useful during early phase of vent support where rest is required

Useful for long term for pt not ready to wean

SIMV

In between positive press breaths pt can breathe spontaneously

Useful for long term for pt not ready to wean

Used as weaning technique for short-term vent dependent pt

PS

Vent functions as constant pressure generator

Positive pressure is set

Pt initiates breath, a predetermined pressure is rapidly established

Pt ventilates spont, establishes own rate, V

T

I:E

, peak flow and

Can be used independently/CPAP/SIMV

Indicated to reduce work imposed by ETT, 5 to 20cm H

2

O

Can be used for weaning

A set IPS (12ml/kg VT) achieved by adjusting IPS level then slowly reducing as clinical status improves

To overcome resistance of ETT, IPS should meet Raw

To determine amount of PS needed: [(PIP – Plateau pressure) / Ventilatory inspiratory flow] x spontaneous peak inspiratory flow

IBW

Estimated ideal body weight in (kg)

Males: IBW = 50 kg + 2.3 kg for each inch over 5 feet.

Females: IBW = 45.5 kg + 2.3 kg for each inch over 5 fee.

1 Kilogram = 2.20462262 Pounds

M ONITORING CMV

Observation

Look at patient!

Make a good visual assessment

Start with patient, trace circuit back to ventilator

Check and drain tubing

Check connections

Check patient

Suctioning, position, etc.

BP

Spontaneous RR

Heart rate and all vital signs

Check machine settings

V

T

(set, exhaled, corrected)

f (assisted, set, spontaneous)

Pressure limit: 10 above delivery pressure

PEEP if applicable: Check BP!

Peak Insp. Pressure (PIP): Keep as low as possible

I:E ratio for proper flow

FiO

2

: Keep as low as possible to prevent Oxygen Toxicity yet keep them adequately oxygenated

Check all apnea alarms and settings.

Check set V

T

 to exhaled V

T for any lost volumes

If difference is greater than 100 cc, check for leak.

Compliance

Measures distensibility of lung – how much does the lung resist expansion.

Relationship between Volume and

Pressure

High compliance equals lower PIP thus easier ventilation and less side effects of CMV

Disease states resulting in low compliance include the Adult Respiratory Distress Syndrome

(ARDS), pulmonary edema, pneumonectomy, pleural effusion, pulmonary fibrosis, and pneumonia among others.

Emphysema is a typical cause of increased lung compliance.

Y

OU MUST KNOW

Dynamic

= VT (corrected or exhaled)

PIP – PEEP

Always subtract out PEEP

Consistently use exhaled or corrected V

T

Used to assess volume/pressure relationships during breathing – any changes in RR will effect it

C

DYN decreases as RR increases which may cause V/Q mismatch which may cause hypoxemia

May reflect change due to change in flow due to turbulence instead of compliance

Normal = 30 – 40 cmH

2

O

V

ERY IMPORTANT

Static

= VT (corrected or exhaled)

Plateau – PEEP

Always subtract out PEEP

Always consistently use either V

T exhaled or V

T corrected

Will not change due to change in flow, more accurate

Measured pressure to keep airways open with no gas flow.

Normal values very with pt, but usually above 80 cmh2o will show lung overdistention

Importance

 to follow trends in patient compliance

Decreased C = stiffer lung = less compliant = higher ventilating pressures = you need a ventilator with high internal resistance to deliver volumes using square wave.

High compliance = possible Emphysema

S TATIC VS D YNAMIC C OMPLIANCE

Decrease in C

DYN with no change in C worsening airway resistance

ST

 indicates

Causes

Bronchospasm

Secretions

Kinked/Occluded ETT

Inappropriate flow and/or sensitivity settings

If both C

DYN problem

 and C

ST worsen, not likely to be an airway

Causes

Pulmonary Edema

ARDS

Tension Pneumothorax

Atelectasis

Fibrosis

Pneumonia

Obesity

Patient Position

RAW = PIP – P plat

Flow (L/sec.)

Airway Resistance

Impedance to ventilation by movement of gas through the airways thus the smaller the airway the more resistance which will increase

WOB (causing respiratory muscle and patient fatigue)

Example: ETT, Ventilator Circuit,

Bronchospasm

Airway Resistance & Compliance

Decreased Compliance + Increased Airway

Resistance = High PIP, Decreased Volumes and significant increase in WOB

Very difficult to wean a patient until problems are resolved

P ATIENT STABILITY

Vital signs

Pulse – normal, weak, thready, bounding, rate, etc.

BP – hypo/hypertensive – directly related to CO

Respirations – tachypnea, bradypnea, hyperpnea, hypopnea, rate, etc.

Color – dusky, pale, gray, pink, cyanotic

Auscultation - bilateral, etc.

Are they bilateral, amount of air moving, rales, rhonchi or wheezing

Are they Vesicular (normal) or Adventitious (abnormal)

Describe what you hear: fine, course, high-pitched, lowpitched, etc.

And the location where you heard it: bilateral bases, posterior bases, right upper anterior lobe, laryngeal, upper airway, etc.

H EMODYNAMIC MONITORING

BTFDC

Also known as

Balloon Tipped Flow Directed Catheter

Swan-Ganz Catheter

Pulmonary Artery Catheter

Done by inserting a BTFDC into R atrium, thru R ventricle, and into pulmonary artery

SvO

2 is drawn from the distal port of a BTFDC

Used to monitor tissue oxygenation and the amount of O2 consumed by the body

C ATHETERS AND I NSERTION S ITES

PA P RESSURE W AVEFORMS

CVP

Monitors fluid levels, blood going to the right side of heart

Normal = 2 – 6 mmHg (4 – 12 cmH

2

O)

Increased CVP = right sided heart failure (cor pulmonale), hypervolemia (too much fluid)

Decreased CVP = hypovolemia (too little fluid), hemorrhage, vasodilation (as occurs with septic shock)

PAP

Pulmonary Artery Pressure = B/P lungs

Monitors blood going to lungs via Swan-Ganz catheter

(BTFDC)

Normal 25/8 (mmHg)

Increased PAP= COPD, Pulmonary Hypertension, or

Pulmonary Embolism

PCWP

Pulmonary Capillary Wedge Pressure monitors blood moving to the L heart

Balloon is inflated to cause a wedge

Normal PCWP = 8 mmHg

Range is 4 – 12 mmHg

Increased PCWP = L heart failure, CHF

Measure backflow resistance

Cardiac Output

Expressed as QT or CO (QT= Greek alphabet, 1050 BC scientist used qt had cardiac output expression)

Normal = 5 LPM

Range 4 – 8 LPM

Decreased CO = CHF, L heart failure, High PEEP effects

I & O

Needs to be monitored closely to prevent fluid imbalance due to increased ADH production and decreased renal perfusion

Fluid imbalance can develop into pulmonary edema and hypertension

C ARDIAC O UTPUT (CO)

The amount of blood pumped out of the left ventricle in 1 minute is the CO

A product of stroke volume and heart rate

Stroke volume: amount of blood ejected from the left ventricle with each contraction

Normal stroke volume: from 60 to 130 ml

Normal CO: from 4 to 8 L/min at rest

Fick CO: Vo2/Cao2-Cvo2

C(a-v)O2 could decrease if CO is increased due to less oxygen needs to be extracted from each unit of blood that passes

Fick Method

The Fick method requires that you be able to measure the A-V oxygen content difference and requires that you be able to measure the oxygen consumption. An arterial blood gas from a peripheral artery provides the blood for the

CaO2 measurement or calculation while blood from the distal PA port of a Swan-Ganz catheter provides the blood for the CvO2 measurement or calculation

Dilution methods mathematically calculate

(using calculus) the cardiac output based on how fast the flowing blood can dilute a marker substance introduced into the circulation normally via a pulmonary artery catheter.

(injecting a dye in prox port of Swanz. Not really used anymore due to infections

M EASURES OF C ARDIAC O UTPUT AND

P UMP F UNCTION

• C

ARDIAC INDEX

(CI)

Determined by dividing the

CO by body surface area

Normal CI is 2.5 to 4.0

L/min/m

2

CI measurement allows a standardized interpretation of the cardiac function

True cardiac output compared to each pers

ON

M EASURES OF C ARDIAC O UTPUT AND

P UMP F UNCTION ( CONT ’ D )

Cardiac work

A measurement of the energy spent ejecting blood from the ventricles against aortic and pulmonary artery pressures

It correlates well with the amount of oxygen needed by the heart

Normally cardiac work is much higher for the left ventricle

M EASURES OF C ARDIAC O UTPUT AND

P UMP F UNCTION ( CONT ’ D )

Ventricular stroke work

A measure of myocardial work per contraction

It is the product of stroke volume times the pressure across the vascular bed

Ventricular volume

Estimated by measuring end-diastolic pressure

Measures of Cardiac Output and

Pump Function (cont’d)

Ejection fraction

The fraction of end-diastolic volume ejected with each systole; normally 65% to 70%; drops with cardiac failure

D ETERMINANTS OF P UMP F UNCTION

Preload

Created by end-diastolic volume

The greater the stretch on the myocardium prior to contraction the greater the subsequent contraction will be

When preload is too low, SV and CO will drop

This occurs with hypovolemia

Too much stretch on the heart can also reduce SV

Determinants of Pump Function

Afterload

Two components: peripheral vascular resistance and tension in the ventricular wall

Created by end systolic volume

Increases with ventricular wall distention and peripheral vasoconstriction

As afterload increases, so does the oxygen demand of the heart

Decreasing afterload with vasodilators may help improve SV but can cause BP to drop if the blood volume is low

Ventilation Patient Parameters

Spontaneous V

T

Is it adequate for patient?

Spontaneous volumes should be between 5 – 8 ml/Kg of

Ideal Body Weight (IBW)

Spontaneous VC

10 – 15 ml/Kg IBW

NIF/MIP/MIF/NIP

-20 to -25 cmH

2

O within 20 seconds

ABG S

PaO

2 represents oxygenation – adjust with

PEEP or FiO

2

PaCO

2 or RR represents ventilation – adjust with V

T pH represents Acid/Base status

 pH acid: High CO

2

(Metabolic cause)

(respiratory cause) or low HCO

3

 pH alkaline: Low CO

2

(Metabolic cause)

(respiratory cause) or high HCO

3

Draw ABGs

To stabilize

With any change in ventilator settings change only one vent setting at a time

With any change in patient condition

V ENTILATOR ALARMS

Appropriate for each patient

Usually 10 higher/lower than set parameter

For pressure and RR settings

V

T alarms 100 ml higher/lower than set V

Adjust all alarms for patient safety.

T

XRAY WHEN INDICATED FOR

Tube placement: 2 – 4 cm above carina

Possible pneumothorax

To check for disease process reversal, or lack of, for treatment purposes and weaning

F REQUENCY OF VENTILATOR CHECKS

Must be done as often as required by the patients condition unstable patients continuous to hourly

In general patients and ventilators need evaluation Q1-Q4h

With every vent check, patient assessment should take place

Use VT exhaled for calculations.

Corrected VT = exhaled vt-tubing lost volume

Tubing volume lost factor 1-8 cc x pressure

Exhaled vt 650= pip-peep x (3) = 60

650-60=590 corrected vt

W AVEFORM A NALYSIS

Three wave forms typically presented together

Pressure

Flow

Volume

Plotted versus time

Horizontal axis is time

Vertical axis is variable

Other common wave forms:

Pressure vs Volume

Flow vs Volume

Pressure vs Time Assessment

Patient Effort: Negative pressure deflection at beginning of inspiration indicates patient initiated breath

Peak & Plateau Pressures

Adequacy of inspiratory flow: If pressure rises slowly, or if curve is concave, flow is inadequate to meet patient’s demand.

Flow vs Time Assessment

Inspiratory flow patterns

Air Trapping – a.k.a. AutoPEEP – expiratory flow fails to reach baseline prior to delivery of next breath

Airway Resistance

Lower slope (smaller angle) indicative of high resistance to flow

Steeper slope (greater angle) indicative of lower resistance to flow

Also increased resistance manifests itself as decreased peak expiratory flowrate (depth of expiratory portion of flow pattern) with more gradual return to baseline as expiratory flow meets with resistance

Bronchodilator = increased peak expiratory flow rate with quicker return to baseline

Volume vs Time Assessment

V

T

= peak value reached during inspiration

Air Trapping = fails to reach baseline before commencement of next breath

Identifying breath type

Larger volumes = mechanical breaths

Smaller volumes = spontaneous breaths

Pressure vs Volume Loop

Volume on vertical axis

Pressure on horizontal axis

Positive pressure on right of vertical axis

Indicates mechanical breath

Application of positive pressure to the lung

Tracing is in a “counter-clockwise” rotation

Subambient pressure to the left of the vertical axis

Indicates a spontaneous breath

Spontaneous inspiration is to the left of the vertical axis

– subatmospheric pressure at start of inspiration

(Intrapulmonary pressure = -3 cmH

2

O)

Spontaneous expiration is to the left of the vertical axis –

+3 cmH

2

O intrapulmonary pressure on expiration

Tracing is in a “clockwise” rotation

Useful in helping diagnosing

Alveolar Overdistension = looks like bird’s beak, or the

“Partridge Family” symbol

Increased R

AW

= looks “pregnant” or “fat”

Decreased compliance = looks “lazy” or like it’s lying down

Flow vs Volume Loop

Helpful in assessing changes in RAW, such as after the administration of a bronchodilator

Flow on vertical axis

Volume on horizontal axis

Inspiration is top part of loop, expiration on bottom

When R

AW improved, expiratory flows are greater and the slope of the expiratory flow is greater

To determine patient effort, use the following curves

Pressure vs Time

Pressure vs Volume Loop

Volume vs Time

All show subambient drops in pressure/volume when patient initiates the breath

To determine Auto-PEEP, use

Volume vs Time

Flow vs Time

Pressure vs Volume Loop

For all curves, ask “does the exhalation reach baseline before the next breath starts

To determine the adequacy of inspiratory flow

Pressure vs Time = concave or slow rise to pressure means inadequate flow on inspiration

Volume vs Time = Too slow flow = increased I – Time = decreased E-Time = AutoPEEP

Volume vs Pressure = Slope is shallow, may look similar to loop associated with increased R

AW

If you detect the patient actively working during mechanical breath, increase the flow to help meet the patient’s demand and decrease the WOB

To assess changes in compliance, use

Pressure vs Volume Loop

Steeper slope = increased compliance, or larger volume at lower pressure

Shallow slope = decreased compliance, or smaller volume at higher pressure

To assess changes in R

AW

, use

Pressure vs Volume Loop

Space – “hysteresis” – between inspiratory and expiratory portions of loop

“Bowed” appearance – inspiratory portion more rounded and distends toward the pressure axis

Flow vs Volume Loop

Observe peak flow on Flow-Volume Loop

Increased R

AW

= Decreased Peak Flow

UNIT B

Acute & Critical Care

PEEP/CPAP

PEEP – Positive End Expiratory Pressure

Definition

Application of pressure above atmospheric at the airway throughout expiration

Goal

To enhance tissue oxygenation

Maintain a PaO

2 above 60 mmHg with least amount of supplemental oxygen

Recruit alveoli

DECREASE (PA-a)02

Don’t forget (PA-a)02 will increase with v/q or shunt

HOW TO ACHIVE CPAP/PEEP

A. Exhaling through a spring tension diaphragm

B. Exhaling through a column of water

C. Exhaling through a partially inflated exhalation valve (mushroom type)

D. A continuous flow through the circuit

Indications

Cardiogenic pulmonary edema

Left sided heart failure

Prevents transudation of fluid

Improves gas exchange

ARDS

Increases lung compliance

Decreases intrapulmonary shunting

Increases FRC

Refractory hypoxemia

PaO

2

< 50 mmHg with an FIO

Increase FRC

2

Opens collapsed alveoli

Increases reserve

>50%

Contraindications

Unilateral lung disease

Hypovolemia

Hypotension

Untreated pneumothorax

Increased ICP

Hazards

All of the effects of CMV are magnified

Increased intrathoracic pressure

Decreased venous return

Increased ADH

Decreased blood pressure

Decreased cardiac output

Loss of thoracic pump

Barotrauma

Physiological effects

Baseline pressure increases

Increased intrapleural pressures

Increased FRC—recruiting collapsed alveoli

Dead space—increased in non-uniform lung disease and healthy lungs by distending alveoli

Increased alveolar volumes

Can increase compliance

Cardiovascular

Decrease venous return

Decrease cardiac output

Decrease blood pressure

Decreases intrapulmonary shunt

Increases mixed venous value (PvO

2 pulmonary artery via Swan-Ganz

)--Drawn from

Increased intracranial pressures

Decrease in A-a gradient (A-a DO

2

)

Increased PaO

2

Decrease in FIO

2

, which causes a decrease in PAO

2

I NITIATION AND MONITORING OF PEEP

Start off at 5 cmH

2 cmH

2

O increments

O and increase by 3 to 5

Adjust sensitivity

With an increase in baseline pressure the sensitivity must be increased or the patient will have to increase inspiratory effort to initiate a breath

Monitor

Blood pressure: First thing you look at when adding PEEP

Cardiac output: Goal is least cardiac embarrassment with the best PaO

2 and least FIO

2

Pulse

If the patient is hypoxemic their heart rate is probably increased

With addition of PEEP the hypoxemia should resolve and pulse should decrease to normal level

PaO

2

: Goal is best PaO

2

FIO

2 with the lowest possible

M AINTENANCE LEVEL OF PEEP

PEEP trial

Used to determine best level of PEEP

This is the pressure at which cardiac output and total lung compliance is maximized,the V

PaO

2 and PvO

2

D

/V

T is minimal, and the best

, and the lowest P(A-a)O

2 are obtained

Optimal Peep

Level at which physiological shunt (Qs/Qt) is lowest without detrimental drop in cardiac output

A C(

A-V

)O

2 of less than 3.5 vol% should reflect adequate CO

Fick’s law CO = VO

2

/C( a-v

)O

2

Cardiac output and C( a-v

)O

2 are inversely related

Best oxygenation with lease cardiac issues

CPAP

Physiologically the same as PEEP

Used in spontaneously breathing patients

Maintains continuous positive airway pressure during inspiration and expiration

Accomplished by a continuous flow of gas or a demand valve

System flow must be enough to meet patient’s peak inspiratory demands

Used to treat OSA

CPAP delivered via mask or nasal pillows

No machine breaths, all spontaneous ventilation

NPPV (B I PAP)

Similar to CPAP

Delivers two levels of pressure during the inspiratoryexpiratory cycle

Delivers higher pressure on inspiration

Delivers lower pressure on exhalation

Less resistance to exhalation

Two levels of pressure

EPAP

Constant pressure delivered during exhalation

Same as CPAP

Adjust for oxygenation

IPAP

Constant pressure delivered during inspiration

Same as IPPB

Adjust for ventilation

The difference between the two pressures is known as pressure support

Used to treat OSA

Better tolerated than traditional CPAP

Delivered with mask or nasal pillows

Used in acute respiratory failure

Can prevent or delay intubation and CMV

Improves ventilation and oxygenation

Improves patient comfort

R ULES OF PUTTING PATIENT ON PEEP

Obtain order

Set-up PEEP and make additional changes

(i.e., sensitivity)

Monitor patient for hazards, BP, CO if available

Monitor for "optimal/best PEEP"

60-60 Rule: to improve oxygenation increase fio2 to 60% then start adding peep (to prevent o2 toxicity). To remove peep go down to 60% and then start removing peep

IMV/SIMV

Definitions

IMV: Intermittent Mandatory Ventilation

Patient receives set number of mechanical breaths from the ventilator. In between those breaths, the patient can take their own spontaneous breaths at a rate and VT of their choice.

SIMV: Synchronized Intermittent Mandatory

Ventilation

Same as IMV, except the mechanical breaths are synchronized with the patient’s spontaneous respiratory rate. Helps improve patient/ventilator synchrony and helps prevent “breath stacking” (where the vent delivers the machine set VT on top of the patient’s spontaneous VT)

IMV

Advantages

Prevents muscle atrophy – makes patient assume an increasing, self-regulating role in their own respirations, helping to rebuild respiratory muscles

Allows patient to reach baseline ABGs – baseline means the patient’s baseline ABGs

Chronic CO of 40

2 retainer ABGs do not have a normal PaCO

2

Decreases mean intrathoracic pressure – the lower the

IMV/SIMV rate, the lower the intrathoracic pressure

Avoids decreased venous return – lower intrathoracic pressure = greater venous return

Avoids cardiac embarrassment – greater venous return = less decrease in cardiac output and blood pressure

May avoid positive fluid balance

Allows normalization of ADH production

Helps avoid cardiac embarrassment

Psychological encouragement

Some patients may exhibit anxiety, especially those who have been on the vent for several days or weeks

Do not tell the patient they will never need the vent again

Some patients become encouraged by progress, being able to do more for themselves

Weaning gradually – re-evaluate if weaning takes several days

May allow decreased use of pharmacological agents – e.g., morphine, diprivan, versed, etc.

If patient is too sedated, won’t be able to breathe spontaneously and participate in weaning

May be the only way to correct respiratory alkalosis on patient who is “over-breathing” the vent in A/C mode

Patient’s spontaneous V

T that of the set V

T will most likely be smaller than on mechanical ventilator

Candidates for IMV/SIMV

IMV/SIMV is great for weaning patient from CMV

Allows patient to assume increased responsibility for providing own respirations, with diminishing mechanical support

Allows patient to re-build respiratory muscle strength

Patient must be stable. Not ideal for unstable patient.

Consider patient unstable if

Fever – causes increased O2 consumption and increased

CO

2 production, thereby increasing WOB

Unstable cardiac status

Unresolved primary problem that caused them to be on the vent in the first place

Problems of IMV

Fighting the ventilator – patient becomes out of phase – or synch – with the ventilator

Stacking of breaths is not necessarily a problem

Patient will normally synchronize self with ventilator rate

Patient disconnection from gas source (with external IMV circuit)

Other problems of CMV

Benefits of SIMV – Synchronized IMV

Prevents stacking of breaths (pt can breath spontaneously through demand valve)

May help patient to become in phase with vent

Breath stacking could be prevented just by increase

inspiratory flow

I NSPIRATORY P RESSURE S UPPORT (IPS)

Commonly referred to simply as “Pressure

Support”

During spontaneous breathing, the ventilator functions as a constant pressure generator

Pressure develops rapidly in the ventilator system and remains at the set level until spontaneous inspiratory flow rates drop to 25% of the peak inspiratory flow (or specific flow rate)

This mode may be used

Independently

With CPAP

With SIMV

With any spontaneous ventilatory mode

Not with any full support modes, such as Control or A/C

PS is used to overcome the increased resistance of the ET tube and vent circuit

Pouiselle’s Law: decrease the diameter of a tube by ½, increase the resistance of flow through that tube by 16 times

If you apply/use PS, do not set less than 5 cmH

2

O of PS — least amount needed to overcome resistance of ET tube and vent circuit

If PS is set at a level higher than RAW, you will be adding to patient volumes, rather than just helping overcome the increased resistance from the ET tube and vent circuit

Can be used to help wean patient from vent and help rebuild respiratory muscle strength

M ANAGEMENT OF VENTILATORS BY ABG S

Pressure Control Ventilation

Can be used as CMV or SIMV

In SIMV mode, the machine breaths are delivered at the preset pressure while the spontaneous breaths are delivered with PS

PC-CMV (a.k.a., PCV) used to decrease shear forces that damage alveoli whenever the peak or plateau pressures meet or exceed 35cm H

2

O

Help prevent damage to alveoli from excessively high ventilating pressures

Shear forces damage alveoli when they collapse (because closing volumes are above FRC) and then are forced back open again with the next breath. Damage occurs as this cycle is repeated over time: alveoli collapses, then is reinflated, collapses, reinflated, etc.

Also used when permissive hypercapnia is desired (treatment of ARDS)

When the PaCO

2 is allowed to rise through a planned reduction in PPV, which allows for a reduction in the mean intrathoracic pressure, which results in less incidence of barotrauma and other commonly associated complications of PPV

The gradual increase in PaCO

2 is accomplished by a reduction of the mechanical VT (by decreasing the pressure) and usually does not affect the oxygenation

PC-IRV: Pressure Controlled Inverse Ratio

Ventilation

Pressure controlled ventilation with an I:E ratio > 1:1.

Causes mean airway pressure to rise with the I:E ratio

Usually used on patients with severe hypoxemia where high

F

I

O

2 s and PEEP have failed to improve oxygenation

Causes intrinsic PEEP (a.k.a. auto-PEEP), which is what causes the mean airway pressure to increase, which is the mechanism for alveolar recruitment and improved arterial oxygenation

While an increase in oxygenation does occur at the lung, a resultant decrease in cardiac output (due to the increased mean intrathoracic pressures) may result in an overall decrease in tissue oxygenation. Care must be exercised to maintain adequate cardiac output in order to maintain adequate tissue oxygenation

Because it’s not a natural way to breath (backwards from the way we normally breath), most patients must be either heavily sedated (Diprivan, Versed) or must be paralyzed with a paralytic drug (such as Pavulon or Norcuron)

APRV: Airway Pressure Release Ventilation

Related to PC-IRV except that patient breathes spontaneously throughout periods of raised and lowered airway pressure.

APRV intermittently decreases or releases the airway pressure from an upper CPAP (IPAP) level to a lower CPAP

(EPAP) level

The airway pressure release usually lasts 1.5 seconds or shorter, allowing the gas to passively leave the lungs to eliminate CO

2

I:E ratio is usually > 1:1, but differs from PC-IRV in that it allows spontaneous breathing

Because patient is breathing spontaneously, there is less need for sedation

Usually has lower peak airway pressure than PC-IRV

Originally proposed as a treatment for severe hypoxemia, but appears to be more useful in improving alveolar ventilation rather than oxygenation.

E ND T IDAL CO

2

M ONITORING (P

ET

CO

2

)

Measures CO

CO

2

2 level at end exhalation, when levels are highest in exhaled breath

Two methods of collection

Sidestream – typically used for non-intubated patients

Mainstream – typically used for intubated patients and more commonly seen and used

Probe is placed between the patient wye of vent tubing and the patient’s ETT

Infrared light measures CO

2 levels

Inspired gas should have value of zero

P

ET

CO

PaCO

2

2

 content should be within 2 – 5 mmHg of patient’s

Difference will be greater on a patient with larger amounts of air trapping, e.g. Emphysema

C

APNOMETRY

(

CONT

.)

End-tidal CO

2

 monitoring is for trending

Not absolute—can vary from breath to breath; similar to pulse oximetry

Look at the trend. Is the patient’s P

ET

CO

2 increasing or decreasing over a period of time? Similar activity should then be also occurring with the PaCO

2

When setup, correlate the P

ET

ABGs PaCO

2

P

ET

CO

2

CO

2 readings with current

. This will give you an idea of how much less the is reading than the PaCO

2

, giving you a good idea of future trends of the P

ET

CO

2 will relate to the PaCO

2

C HEST T UBE D RAINAGE S YSTEMS

Chest tube placed high in thoracic cavity to drain air

Second or third intercostal space at midclavicular line

Incision made right over the rib

Chest tube advanced towards anterior apex of lung.

Chest tube placed low in thoracic cavity to drain fluid (e.g., pleural effusion)

Placement is in fourth intercostal space (or lower) at midaxillary line

Patient is placed lying on side with affected side “up”

Once incision is made, tube is advanced posteriorly, toward the base of the lung so gravity can help drain the fluid

Three chamber chest tube drainage system is most common

Left chamber is the suction control chamber

Level of water determines how much suction is applied to the chest cavity, regardless of how much the suction is set on the suction regulator on the wall

Middle chamber is the water seal chamber

Usually no more than 2 cmH

2

O

Too much and you increase difficulty of air or fluid to drain

Too little and you risk an air leak

Bubbles in water seal indicate that a leak in the lung is still present

Spontaneous breathing patients with leak will have bubbles on exhalation

Intubated, mechanically ventilated patients with leak will have bubbles on inspiration

Continuous bubbling could be a sign of a leak in your chest tube drainage system and must be corrected immediately!

Clamp chest tube briefly where it exits patient’s chest. If bubbling stops, leak is in your patient (intrathoracic).

If bubbling persists, then you must check your chest tube drainage system for leaks

Move clamp down tubing in 10cm (approx. 4 inch) increments

(working from patient to chest tube drainage system), briefly clamping as you go until bubbling stops

Right chamber is the drainage collection chamber

This is where the fluid drained from the patient is collected

ALI=A CUTE LUNG INJURY OR ARDS

Definition agreed upon in 1994 at the American –

European Consensus Conference on ARDS

ALI Definition: a syndrome of acute and persistent lung inflammation with increased vascular permeability. Characterized by:

Bilateral radiographic infiltrates

A ratio PaO

2

/F

I

O

2 between 201 and 300 mmHg, regardless of the level of PEEP. The PaO

2 the F

I

O

2 is measured in mmHg and is expressed as a decimal between 0.21 and 1.00

No clinical evidence of an elevated left atrial pressure. If measured, the PCWP is 18 mmHg or less

ARDS Definition: same as ALI, except the hypoxia is worse. Requires a PaO

2

/F

I

O

2 ratio of

200 mmHg or less, regardless of the level of

PEEP. ARDS is ALI in its most extreme state

Mortality rate between 40 and 60%

-varies from source to source

Down from about 20 years ago when ARDS was almost certain death sentence with approximately 90% mortality rate.

Current Protective Lung Strategies

Lower V

T s with ALI/ARDS patients: about 6 ml/Kg IBW to avoid “volutrauma” from alveolar over distension

Sufficient PEEP to prevent alveolar collapse at end expiration, yet not so much that cardiac status is compromised

Permissive hypercapnia when treating

ALI/ARDS

PaO

2

> 65 mmHg

PIP < 35cm H

2

O

If your PIP is greater than 35cm H

2

O, consider using PCV

Closed suctioning system to maintain PEEP

Do not “bag” ALI/ARDS patient to “recruit more alveoli”; could lead to barotrauma or volutrauma

Monitor: Patient must be monitored closely as condition can change relatively quickly!

Things to monitor:

I&O

Cardiac output

BP

PIP

P

PLAT

Pulse Ox

F

I

O

2

V

T

V

E

CST

P

ET

CO

2

Waveforms

A-a Gradient

Renal vasoconstriction, due to hypoxemia, reduces urinary output.

Resolution of the hypoxemic state relieves the renal vasoconstriction, thus increasing urinary output.

M ANAGEMENT OF ABG S WITH CMV

ABG normal pH values

Normal range = 7.35 – 7.45

“Normal” = 7.40

PaCO

2

High PaCO

2 acidosis

Low PaCO

2 alkalosis will cause a low pH, thus causing respiratory will cause a high pH, thus causing respiratory

 pH needs to be corrected so that drugs being given to patient will be metabolized

PaCO

2

 and Ventilation

ABG normal PaCO

2 values

PaCO

2

/Ventilation = 35 – 45

“Normal” = 40

High PaCO

2 represents hypoventilation or the patient is under ventilated or retaining CO

2

Low PaCO

2 represents hyperventilation or the patient is over ventilated or blowing off CO

2

CO

2 represents how well your patient is ventilating. You would adjust V

T

, f, or remove dead space if on ventilator

PaCO

2

PaCO

2

& pH Calculations and pH have a direct relationship.

Starting at a PaCO

2

If PaCO

2 of 40 increases by 20 mmHg, pH decreases by 0.10

If PaCO

2 decreases by 10 mmHg, pH increases by 0.10

To increase PaCO

2

 decrease VA

The PaCO

2

CO

2 is inversely proportional to VA providing that production remains constant

VA = (V

T

– V

D

)f

To decrease VA (increase PaCO

2

Decrease V

T

(keep in normal range)

)

Decrease f (will not blow off as much CO

2

)

Increase V

D bore tubing)

(only in control mode – 50cc per link of large

To decrease PaCO

2

VA = (V

T

– V

D

)f

 increase VA

To increase VA (decrease PaCO

2

)

Increase V

T

(keep in normal range)

Increase f (will blow off more CO

2

)

Decrease V

D

Dead Space = Ventilation without perfusion

Anatomical dead space averages about 1 ml per pound

Alveolar dead space is alveoli that are ventilated but not perfused

Physiological dead space is the sum of the above

Normally, this is approximately 1/3 of the V

T

, or between

20 and 40% for spontaneously breathing, non-intubated patient

Normal for patient on ventilator is 40 – 60%

Formulas for V

D

/V

T

, Desired V

T

, & Desired f

V D /V T = PaCO2 – PetCO2

PaCO2

Gives the portion/percentage of V

T exchange.

not taking place in gas

S TRATEGIES TO ALTER VENTILATION

Always adjust V

T first, but remember to keep it in the normal range (8 – 12 ml/kg of ideal body weight)

If PaCO

2 is high, patient is on SIMV, and the patient is taking spontaneous breaths and the volumes are low, initiate Pressure Support to increase spontaneous volumes.

If you cannot adjust V

T the V

T up or down because it would place out of normal range, then change f (rate)

Change Mechanical Rate

Doing this alters Alveolar Ventilation

If your rate exceeds 20 bpm, auto-PEEP may develop

(patients with very stiff lungs. e.g., ARDS—may require higher f)

Increase f = decreased PaCO

2

Decrease f = increased PaCO

2

(hyperventilate)

(hypoventilate)

Add or remove V

Add V

DMech

DMech only in control mode to increase PaCO

2

Decrease V

DMech to decrease PaCO

2

Cut ETT to proper length to decrease dead space

Use low compliance vent circuit to decrease dead space

Large V

T and slow f are preferred to small V and rapid f because

T

Alveolar Ventilation is increased

Distribution of inspired gas is improved

Ventilation/Oxygenation is improved

Mean intrathoracic pressure is reduced

P A O

2

& O XYGENATION

PaO

2

/Oxygenation norm = 80 – 100

If PaO

2 is below 60, the patient has hypoxemia

For patients that are hypoxic and on a ventilator, adjust the F

2 to > 50% then start adding PEEP

I

O

When the patient improves, decrease F

I

O

2

40 – 50%, then start removing PEEP to prevent O

2 toxicity to

To increase PaO

2

(in any mode)

Increase F

I

O

2 if hypoxemia is caused by low

V/Q ratio to > 50%, then add PEEP to prevent oxygen toxicity. (  )

What is oxygen toxicity? How does it effect the patient?

When hypoxemia is present due to lung injury or physiological shunting (as in disease states like ARDS), add PEEP or CPAP

PaO

2 can be altered by either reducing or increasing PaCO levels by controlling VT

2

By reducing PaCO

2 levels (hyperventilation), PaO increase (RBCs can carry more O

2

)

2 levels

Works the opposite way, too—increasing PaCO

2 levels (hypoventilation), PaO2 levels decrease

(RBCs carry less O

2

)

T WO INDICES OF OXYGENATION

 a/A Ratio

PaO

2

/PAO

2

O

2 from alveoli to blood

Divide PaO

2 by PAO

2

Normal = > 60%

A-a Gradient

P

(A-a)

O

2

Difference between alveolar and arterial PO

2

Also known as: - D(

A-a)

O

2

Subtract PaO

2 from PAO

2

Normal: - On 21%: 10 – 15 - On 100%: 65

On 100%, every 50 mmHg difference equals approx. 2% shunt

If under 300, you have V/Q mismatch so increase F i

O

2

If over 300, you have a shunt, so add PEEP or CPAP

First calculate PAO

2

Unless told otherwise

PBAR = 760

PH

2

O = 47

RQ = 0.8

(Pb-PH2O)fio2-(Paco2x1.25)

If F i

O

2 is greater than 60%, omit RQ from PAO2 formula

PaO

2 is obtained from an ABG

To decrease PaO

2

Decrease F

I

O

2

(in any mode)

Decrease PEEP gradually

If F

I

O

2

> 50% with PEEP, decrease F

(to reduce O

2 toxicity)

I

O

2 to 40 – 50% first

If patient remains stable and has an adequate PaO

2 to reduce PEEP slowly

, start

Increase PaCO

2

(Dalton’s Law)

Monitor patient at all times for signs of hypoxemia

M ANIPULATION OF ABG S IN CONTROL

MODE

To increase PaCO

2

Decrease V

T

Decrease f

Increase V

D

To decrease PaCO

2

Increase V

T

Increase f

Decrease V

D

M ANIPULATION OF ABG S IN A/C

To increase PaCO

2

Decrease VT: May be ineffective as pt. may increase f

Decrease f: Patient can increase assisting to override

Never add V

D in any mode but control

To decrease PaCO

2

Increase V

T

Increase f above assist rate

If ineffective, change to control or IMV modes

M ANIPULATION OF ABG S IN SIMV/IMV

To increase PaCO

2

Decrease V

T

– only to ranges for patient

Not best choice

Decrease f

Best choice towards weaning

Never add V

D in this mode

Will increase patient’s WOB and they will eventually fail

To decrease PaCO

Increase V

T

2

- stay within normal range

Increase f (blow off CO

2

)

Increase minute ventilation

May need to add PS to augment spontaneous volumes

Do not look at just the numbers and values

Always assess your patient with every ventilator change.

You are treating a patient, not a machine!

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