Objectives - img1.wsimg.com

2/28/2022

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OXYGEN THERAPY

KELLY URBAN, PHD, MED, RN, CCRN-K, TCRN

UAMS

NASAL CANNULA

Run on 1-6 LPM of flow

Any flow of 4-6 LPM should be humidified for patient comfort and to avoid drying out the nasal mucosa

Percentage of oxygen delivered to the patient is varied depending on the patient’s depth of breathing. The larger the breath the lower the FiO2 delivered.

There is an approximation of FiO2 delivered by a Nasal Cannula based on the liter flow

1 LPM ~ 24% 4 LPM ~ 36%

2 LPM ~ 28% 5 LPM ~ 40%

3 LPM ~ 32% 6 LPM ~ 44%

AIR ENTRAINMENT MASK

Provides a fixed percentage of oxygen ranging from 24% to 50%

Two types of devices:

1: Has multiple jet pieces that each provide a specific FiO2

2: Has a rotating adaptor that controls the air entrainment window

These devices are good for CO2 retainers who require a fixed FiO2 and higher flows of O2

NON-REBREATHER

Gives up to 100% FiO2 when flowmeter is turned up to “flush”

May not be able to give 100% if the patient is taking very large breaths

Devise has a reservoir bag and

a one way valve. The one way

opens during inspiration

allowing the oxygenated air

into the mask and

closes during expiration so

that oxygen refills the bag

during expiration, instead of CO2

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HIGH FLOW NASAL CANNULA

High Flow Nasal Cannula

Provides flows for 2 LPM to 12 LPM

Requires humidification

COMFORT FLOW NASAL CANNULA

Comfort Flow Nasal Cannula

Provides flows up to 40 LPM

Provides a fixed FiO2 via an oxygen/air

blender

Must be heated and humidified

Great alternative for hypoxic respiratory failure

BIPAP/CPAP

CPAP-Continuous Positive Airway Pressure Provides continuous pressure to keep the alveoli open on exhalation to improve oxygenation

Used to treat conditions, such as fluid overload and obstructive sleep apnea

BiPAP- Bilevel Positive Airway Pressure Provides CPAP as well as IPAP (Inspiratory Positive Airway Pressure)

The IPAP assists the patient with taking a deeper breath which can improve Co2 removal (this is not considered a “ventilator”, it only enhances the patients spontaneous breath)

**PATIENTS MUST BE ABLE TO SPONTANEOUSLY BREATHE FOR BiPAP OR CPAP TX.

CARE OF THE MECHANICALLY VENTILATED PATIENT

TAMMYE WHITFIELD, MED, RRT

EDUCATION COORDINATOR

RESPIRATORY CARE SERVICES

UAMS

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OVERVIEW

Artificial Airways

Types

Placement

Management

Trouble Shooting

Mechanical Ventilation

Modes

Management

Trouble Shooting

Weaning

Post Extubation Care

CONDITIONS THAT REQUIRE ARTIFICIAL AIRWAY

Obstruction in the airway

Upper airway swelling

i.e. Mass/Tumor

Protection of the airway due to failure of normal protective mechanisms

No gag reflex

Glottis malfunction

Decreased neurological function

To enable mechanical ventilation

TYPES OF AIRWAYS

Oral Endotracheal Tube

Advantages:

Most commonly used in the hospital

Easy placement and removal

Good for short term airway use

Disadvantages:

Oral care is difficult, causing greater risk of infection and pneumonia

Excessive salivation

Coughing and biting due to gag reflex and discomfort

TYPES OF AIRWAYS

Nasal Endotracheal Tube

Advantages:

Good for patients with cervical spine injury

Useful for patients having oral surgery or injuries

Useful in patients who have large oral mass or obstruction

Disadvantages:

Nasal trauma and bleeding risk

Must use smaller tube

Can block Eustachian tube and sinuses possibly causing inflammation and swelling

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TYPES OF AIRWAYS

Laryngeal Mask Airway

Advantages:

Easy to place correctly

Good for short term use in the field and the OR

Disadvantages:

Difficult to maintain proper placement over long periods of time

Can cause irritation and tissue damage

TYPES OF AIRWAYS

Tracheostomy Tube

Advantages:

More Comfortable

Less aspiration of oral secretions

Facilitate gradual weaning for patients who have had multiple weaning failures

Disadvantages:

Surgical procedure with risk of bleeding and infection

Permanent incision must have time to heal once trach is no longer needed

Can cause scarring

INTUBATION EQUIPMENT

Oral airway

Ambu bag and mask

ET tube

Stylet

Layrngoscope handle and appropriate size blade(s)

Flexible suction catheter and Yankauer

10 cc syringe (for cuff inflation)

Tube holder

Water soluble lubricant

Suction unit and canister

End tidal CO2 detector, stethoscope

Ventilator

INTUBATION PROCEDURE

Explain procedure and obtain consent if possible

Select ET tube size and insert stylet (stylet should be completely inside ET tube, not sticking out of the end of the tube)

Select Laryngoscope blade size

Check Laryngoscope blade, light, ET tube cuff, suction, etc…prior to intubation

Administer sedation and ventilate patient with bag and mask as breathing depth and rate decrease (use oral airway if needed)

Position head in sniffing position

Once ET tube is inserted remove stylet, inflate the cuff and begin bagging with ETCO2 detector in place

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INTUBATION CONFIRMATION

Visualization- chest rises equally on left and right

Auscultation- equal breath sounds over both lungs and no air heard in the stomach

ETCO2 detector-good color change indicates CO2 or good CO2 range via monitor

Chest X-Ray- ET tube has radiopaque line that should end 3-5 cm above the carina

AIRWAY CONFIRMATION AND MONITORING

Capnography- the continuous measurement of exhaled CO2

Normal etCO2= 35-45 mmHg

AIRWAY MANAGEMENT

ET Tube

Resuscitation bag and mask should be at bedside and visible

An ETT holder should be in place and should be changed when it is soiled or the adhesive is worn off

Tube placement should be checked and documented each shift as well as after the patient is moved or turned

Oral care should be performed frequently

Cuff pressure should be monitored (normal= 20-30 mmHg)

Pt should be restrained as needed

TrachTube

Obturator, resuscitation bag and mask should be kept at the bedside and visible

An extra trach tube should be avail.

Trach should be secured by trach ties which should be changed when soiled

Trach site condition should be observed and documented each shift

Trach care should be performed each shift

Oral care should be performed frequently

Cuff pressure should be monitored

Pt should be restrained as needed

AIRWAY TROUBLESHOOTING

Problem

Audible air leak from pt’s mouth

Possible Cause

Cuff is under inflated

Solution

Add air to cuff

Problem

Large air leak around tube that is not fixed when adding air to cuff

Possible Cause

Cuff has ruptured

Pt is extubated

Solution

Suggest exchanging the tube/reintubation

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Problem

Decreased breath sounds in both lungs

Possible Cause

Tube occluded

Kink in tube or circuit

Solution

Suction

Examine tube and circuit for kinks or occlusions

Problem

Decreased breath sounds in one lung

Possible Cause

Main stem intubation

Pneumothorax

Severe atelectasis

Solution

Stat CXR

Withdraw tube based on CXR findings


CONDITIONS THAT REQUIRE VENT SUPPORT

50/50 Rule

Acute severe hypoxemia- PaO2 of less than 50

Acute ventilatory failure- Acidotic- PaCO2 greater than 50 with a pH less than 7.30

Respiratory Muscle Insufficiency

RR greater than 30 BPM

Increased WOB and use of accessory muscles

NIF less than -20 cmH2O (normal=more than -60 cmH2O)

BASIC VENTILATOR MODES: CMV/AC

Continuous Mandatory Ventilation/Assist Control

Set rate and tidal volume (Vt)

Pt can initiate as many breaths as they want but each breath will be given at the set Vt

Used to allow patient to rest

Ventilator does all the work

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BASIC VENTILATOR MODES: SIMV

Synchronized Intermittent Mandatory Ventilation

Set rate and Vt given with each mandatory breath

In between mandatory breaths patient can take their own breath with “pressure support”

Good mode for weaning

Vent does part of the work and pt does the rest (only if the pt makes effort to breathe over the set rate)

BASIC VENTILATOR MODES: CPAP/PS

Continuous Positive Airway Pressure with Pressure Support

Spontaneous mode of ventilation

CPAP stents alveoli open while PS helps to augment Vt

No set rate; patient must initiate all breaths

Can indicate how well the patient will do once extubated

BASIC VENTILATOR MODES: APRV

Airway Pressure Release Ventilation

Used for patient who are unable to oxygenate with traditional ventilation despite high FiO2 and PEEP

Uses inverse ration ventilation to keep lungs openlonger for maximal oxygenation

Risk of pneumothorax, barotrauma, decreased cardiac output

BASIC VENTILATOR SETTINGS

FiO2

Fraction of inspired oxygen

Can deliver room air (21%) and up to 100% as required

Tidal Volume [Vt]

Tidal volume

Volume of air delivered by the vent with each mechanical breath

Respiratory Rate [RR] or Frequency

Respiratory rate

Number of mechanical breaths delivered each minute

PEEP

Positive End Expiratory Pressure

Continuous pressure that keeps alveoli from collapsing at the end of expiration

Pressure Support [PS]

Increase in pressure designed to support the patients own spontaneous breaths, essentially increasing their spontaneous Vt and decreasing resistance applied by ET tube

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VENTILATOR ALARMS

High Pressure

Possible causes

Biting ET tube

Kink in tube or circuit

Occlusion (Suction catheter left in ETT)

Plug (i.e. mucous or blood)

Tension pneumothorax

Pt coughing or bucking the vent

Low Pressure

Possible cause

Pt “popped off” vent; disconnected

Cuff not properly inflated or severe leak in circuit

Pt is extubated

Apnea Alarm

Sounds when patient fails to breath within a preset period of time in a spontaneous vent mode

VENTILATOR MANAGEMENT

What two vent settings control oxygenation?

FiO2 and PEEP

How would you manipulate those settings to improve oxygenation?

What two vent settings control ventilation?

RR and Vt

How would you manipulate those settings to improve ventilation?

VENTILATOR MANAGEMENT

ABG Review Normal pH- 7.35-7.45

Normal CO2- 35-45

Normal HCO3- 22-26

Normal PaO2- 80-100

ABG Interpretation 7.25/68/96/25

7.54/25/75/23

7.20/43/68/17

7.58/40/90/30

WEANING FROM MECHANICAL VENTILATION

Weaning should begin when initial reason for mech. ventilation is resolved!

Wean sedation

Place pt in spontaneous mode of ventilation

Monitor vital signs, Vt, RR and work of breathing

Place back on controlled mode if pt becomes tachypneic or tachycardic or in anyway unstable

If pt passes trial they are probably ready for extubation

Breathing tests or ABG’s can be ordered to further assess pt’s readiness for extubation

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EXTUBATION

Pre-oxygenate with 100% FiO2

Suction down tube and above cuff

Head of bed should about 45 degrees or fowler’s so that patient can deep breathe and cough

O2 device should be set up and ready and Yankauer should be ready with suction on

POST EXTUBATION

No talking for an hour

No food or drink until swallow can be assessed

Vital signs and breath sounds should be closely monitored

Incentive Spirometry should be initiated

Pt should be up in a chair as soon as condition is appropriate

KEY POINTSAirway placement and management

Know tube placement and monitor while turning and cleaning pt

Keep airway suctioned and clean

Ventilator Management Become proficient at ABG interpretation

PREVENTION IS KEY!!! Be proactive

QUESTIONS

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ABGS AND BEYOND: ASSESSING OXYGENATION AND VENTILATION

KELLY URBAN, PHD, MED, RN, CCRN-K, TCRN

UNIVERSITY OF ARKANSAS FOR MEDICAL SCIENCES

DESCRIPTION

Arterial blood gases are used to measure the amount of oxygen, carbon dioxide, and bicarbonate in the blood, as well as the pH.

ABGs provide information regarding physiologic phenomena

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ACIDS

Substances capable of releasing a hydrogen ion (H+) into solution.

Volatile acids excreted through the lungs (CO2)

Fixed or nonvolatile acids excreted by the kidneys (ketoacids and lactic acid)

BASES

Substances capable of combining with H+ in solution.

Bicarbonate (HCO3) Most important base in the blood

regulated by the kidneys

Hemoglobin and plasma proteins.

Bases are reflected in the ABGs as the HCO3 and the base excess or base deficit.

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ACID – BASE BALANCE

Reflection of relationship between bases and acids in the blood

Acid base balance is reflected in the pH

ELEMENTS OF ABGS: NORMAL VALUES

pH--7.35 to 7.45

represents a combined effect of metabolic and respiratory factors.

low pH indicates acidosis

high pH indicates alkalosis

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PCO2--35 to 45 mm HG

A measure of the partial pressure of carbon dioxide dissolved in the plasma.

byproduct of metabolism

CO2 is excreted by the lungs and is a measure of the adequacy of ventilation.

CO2 functions as an acid because it combines with water to produce carbonic acid, H2CO3.


HCO3--22 to 26 mEq/L

Bicarbonate ion is a base regulated by the kidneys

It may be adjusted to compensate for respiratory acid-base imbalance, or may be altered by other factors such as kidney disease or metabolic alterations

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PaO2--80-100 mm Hg

Is the partial pressure of oxygen dissolved in arterial plasma

Only about 1% of total oxygen content is carried in this state, PaO2 indicates how well oxygen is being taken up in the lungs.


SaO2--95 to 98%

SaO2 represents the percentage of total hemoglobin which is saturated with oxygen.

The vast majority of oxygen is carried in this state.

While saturation is usually well-correlated with PaO2, some conditions (pH, temperature) can influence the relationship between these two parameters

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Base Excess (BE) -2 to +2

It represents the combined effects of HCO3 and other bases--plasma proteins, hemoglobin and others

A negative base excess is sometimes referred to as a base deficit.

SUMMARY OF NORMAL VALUES

pH 7.35 – 7.45

PaO2 80 – 100 mmHg

PCO2 35 – 45 mmHg

HCO3 22 – 26 mEq/L

Base Excess (BE) -2 - +2

SaO2 95% - 98%

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STEPS IN ABG INTERPRETATION

1. Check pH acidotic, alkalotic, or normal

2. Check PaCO2 (respiratory parameter) Elevated (acidotic), decreased (alkalotic), or normal

3. Check HCO3 (metabolic parameter) Elevated (alkalotic), decreased (acidotic), or normal

4. If abnormalities exist, determine which of the major acid/base imbalances is present

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STEPS IN ABG INTERPRETATION CONT’D

5. Determine whether any compensation mechanisms are involved

6. Check PO2 and O2 saturation normal, elevated, or decreased

7. Observe patient evaluate vital signs and physical parameters

Evaluate why patient presents any abnormal values which are present and implement appropriate actions to correct the acid/base imbalance

RESPIRATORY ACIDOSIS (ELEVATED PACO2)

Caused by hypoventilation of any etiology COPD

Oversedation, head trauma, anesthesia, or reduced function of respiratory center.

Neuromuscular disease

Inappropriate mechanical ventilation

Other causes of hypoventilation (sleep apnea)

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RESPIRATORY ALKALOSIS (LOW PACO2)

Hyperventilation Hypoxemia

Nervousness and Anxiety

Pulmonary Embolus

Pregnancy

Inappropriate Mechanical Ventilation

Compensation for Metabolic Acidosis

METABOLIC ALKALOSIS (ELEVATED HCO3)

Caused by a loss of nonvolatile acid or increase in HCO3

Gastric loss of acid

HCO3 during cardiac arrest

Baking soda

Massive blood transfusion – citrate – lactate - bicarbonate

Increased excretion of H+, K+, and Cl – due to :1. Diuretics

2. Cushings Syndrome

3. Corticosteroids

4. Aldosteronism

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METABOLIC ACIDOSIS (DECREASED HCO3)

Increase in immeasurable anions:

Diabetic ketoacidosis

Renal failure

Lactic Acid

Poisoning: salicylates, ethylene glycol, methyl alcohol, paraldehyde

No increase in immeasurable anions:

Diarrhea

Drainage of pancreatic juice

Treatment with Diamox

Treatment with ammonium chloride

Renal tubular Acidosis

Caused by a gain in nonvolatile acid which uses up HCO3 or loss of HCO3

CLINICAL SIGNS OF ACIDOSIS (CNS DEPRESSION)

Depressed thought processes

Delayed reaction times

Slurred speech

Somnolence

Incoordination

Confusion

Semi-coma

Death

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CLINICAL SIGNS OF ALKALOSIS (CNS EXCITATION)

Anxiety

Paresthesia

Tremors

Nausea

Tetany

Convulsions

Death

ANION GAP

The anion gap refers to a difference in the routinely measured cations (positively charged particles, such as Na +, Ca++, and Mg ++) and anions (negatively charged particles , such as HCO3

- and Cl-)

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ANION GAP

The formula for the anion gap is:

AG= Na+ - (HCO3- + Cl-)

The normal anion gap is 8-16 mEq/L

ANION GAP

Na 138

HCO3- 11

Cl- 99

AG = Na+ - (HCO3- + Cl-)

138 - (11 + 99)

= 138 - 110

= 28

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ANION GAP – WHY DO WE CARE?

Assists in differential diagnosis of the type of metabolic acidosis

An elevated anion gap acidosis suggests an increase in plasma level of unmeasured cations (accumulation of acids is not adequately buffered by a base)

A nonelevated anion gap acidosis reflects the loss of bicarbonate, rather than an increase in acid production or a decrease in acid excretion.

COMMON DISORDERS OF METABOLIC ACIDOSIS

Metabolic Acidosis with elevated anion gap

MUDPILERS

M – Methanol ingestion

U – Uremia

D – Diabetic, alcoholic, or starvation ketoacidosis

P – Paraldehyde injestion

I – Isoniazid, salicylate, or iron poisoning

L – Lactic acidosis

E – Ethylene glycol ingestion

R – Rhabdomyolysis

S – Salicylates

Metabolic Acidosis with normal anion gap

HARD-UP

H – Hyperalimentation

A – Acetazolamide

R – Renal tubular acidosis, renal insufficiency

D – Diarrhea and diuretics

U – Uteroenterostomy

P – Pancreatic fistula

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RESPIRATORY ACIDOSISPH IS LOW AND PACO2 IS HIGH

pH 7.30

PCO2 65

PO2 90

HCO3- 26

BE 0

SaO2 95%

RESPIRATORY ALKALOSISHIGH PH ALONG WITH A LOW PACO2

pH 7.5

PCO2 30

PO2 90

HCO3- 26

BE 0

SaO2 95%

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METABOLIC ACIDOSISPH IS LOW WITH A LOW HCO3

- AND/OR BE

pH 7.30PCO2 35PO2 92HCO3- 18BE -3SaO2 97%

METABOLIC ALKALOSISHIGH PH ALONG WITH A HIGH HCO3

- AND/OR BE

pH 7.5

PCO2 40

PO2 95

HCO3- 35

BE +3

SaO2 96%

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PHENOMENA

Compensation Body’s ability to regulate pH by adjusting either the rate

of ventilation (excretion of CO2) or the renal excretion of HCO3)

Mechanism by which an abnormal PaCO2 or HCO3 may be accompanied by a normal or near-normal pH

COMPENSATION CONT’D

In other words, it is the body’s attempt to normalize pH.

Common compensatory mechanisms involve regulating the amount of CO2 (respiratory compensation-fast response) or the amount of HCO3- (metabolic compensation-slower response)

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HOW?

Respiratory acidosis due to increased PaCO2 Compensation: Kidneys excrete more acid and less HCO3- resulting in increased HCO3-

Respiratory alkalosis due to decreased PaCO2 Compensation: Kidneys excrete HCO3-

Metabolic acidosis due to decreased HCO3- Compensation: Hyperventilation to decrease PaCO2

Metabolic alkalosis due to increased HCO3- Compensation: Hypoventilation to increase PaCO2

COMPENSATION

Primary Disorder

Cause Compensation Effect on ABGs

Metabolic Acidosis

•Excess nonvolatile acids•Bicarbonatedeficiency

Rate & depth of respirations increase eliminates additional CO2

↓ pH↓ HCO3↓ PaCO2

Metabolic Alkalosis

•Bicarbonate excess Rate & depth of respirations decrease retaining CO2

↑ pH↑ HCO3↑ PaCO2

Respiratory Acidosis

•Retained CO2 &excess carbonic acid

Kidneys conserve bicarbonate to restore carbonic acid : bicarbonate ratio 1:20

↓ pH↑ PaCO2↑ HCO3

RespiratoryAlkalosis

•Loss of CO2 &deficient carbonic acid

Kidneys excrete bicarbonate and conserve H+ to restore carbonic acid : bicarbonate ratio

↑ pH↓ PaCO2↓ HCO3

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COMPENSATION CONT.

There are two types of compensation

Partial Compensation pH, PaCO2, and HCO3 are all abnormal

Full Compenstion pH is normal, PaCO2 and HCO3 are abnormal

ASSESSMENT OF ACID-BASE BALANCE

Look at the pH, and determine if it is low (acidotic), normal, or high (alkalotic)

Look at the CO2 and HCO3 and determine if these values “match” the pH. For example, you would expect a normal pH to go along with a

normal CO2 and HCO3-. A normal pH with abnormal CO2 and HCO3 indicates compensation.

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PARTIAL COMPENSATION

pH 7.18

pC02 34

HC03 12

Pa02 84

Fi02 .21

P/F ratio 400

PARTIAL COMPENSATION

pH 7.22

pC02 59

HC03 35

Pa02 35

Fi02 .21

P/F Ratio 167

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NAME THAT ABG

pH 7.42

PCO2 50

PO2 80

HCO3- 32

BE 2.5

SaO2 95%

NAME THAT ABG

pH 7.37

PCO2 32

PO2 90

HCO3 18

BE -2.5

SaO2 98%

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NAME THAT ABG

pH 7.39

PCO2 64

PO2 65

HCO3 37

Fi02 .30

P/F Ratio 217

NAME THAT ABG

pH 7.45

PCO2 27

PO2 65.5

HC03 19.1

Fi02 .40

SP02 .88

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WHAT ABOUT THIS ONE?

pH 7.20

PCO2 65

PO2 55.5

HC03 12

Fi02 .80

SP02 .88

PHYSIOLOGIC PHENOMENA

Oxygenation

Ability of the lungs to deliver fresh O2 to the blood in the pulmonary capillary beds

Reflected in the partial pressure of oxygen (PaO2) and the percent saturation of oxygen (SaO2) in the arterial blood

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OXYGENATION DEFINITION

Amount of oxygen carried in the arterial blood that is bound to the hemoglobin molecule.

It is reflected as SaO2 (the percent of hemoglobin in saturated with oxygen)

The driving force for SaO2 is the PaO2 (partial pressure of dissolved oxygen in the blood)

ASSESS OXYGENATION

Look at the PaO2, which is a good indicator of O2 uptake in the lungs.

Assess the SaO2 as an indicator of O2 content (CaO2)

While PO2 and SaO2 are related, the vast majority of the total O2 content is reflected in the SaO2

Consider the hemoglobin content of the blood

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PHENOMENA CONT’D

Ventilation Ability of the body to rid itself of carbon dioxide (CO2)

Reflected in ABGs as partial pressure of CO2 (PaCO2)

ASSESS OXYGEN DELIVERY

The ‘bottom line’ of respiration is the delivery of O2 to the body’s cells and removal of carbon dioxide

For this to occur, the oxygenated blood must be delivered to the tissues and deoxygenated blood returned to the heart

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TWO WAYS TO ASSESS O2 DELIVERY

Oxygen delivery and uptake by tissues can be measured using a properly equipped pulmonary artery catheter

Basic physical assessment cues: Short of breath or hyperventilating

Blood pressure, pulse rate and rhythm, skin temperature and color

Distention of the neck veins, Auscultation of a gallop or murmur

Crackles at the bases of the lungs

OXYHEMOGLOBIN DISSOCIATION CURVE

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LET’S SING A SONG…..

PaO2 SaO230 6060 9040 75

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A patient with renal failure has the Following ABG:

pH 7.38PaC02 29HCO3

- 17

This Imbalance is MOST LIKELY:1. Compensated metabolic acidosis2. Compensated respiratory acidosis3. Compensated respiratory alkalosis4. Compensated metabolic alkalosis

A patient has had an NG tube to intermittentSuction for 4 days following abdominal

Surgery, her ABGs are:pH 7.51PaC02 45HCO3

- 31

This Imbalance is MOST LIKELY:1. Compensated metabolic acidosis2. Compensated respiratory acidosis3. Uncompensated metabolic acidosis4. Uncompensated metabolic alkalosis

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A semi-comatose diabetic patient is admitted to The ED with the following ABGs:

pH 7.28

PaC02 35HCO3

- 16

This Imbalance is MOST LIKELY:1. Compensated metabolic acidosis2. Compensated respiratory acidosis3. Uncompensated metabolic acidosis4. Uncompensated metabolic alkalosis

A patient suspected of over-dosing hasThe following ABG’s:

pH 7.24

PaC02 65HCO3

- 22

This Imbalance is MOST LIKELY:1. Compensated metabolic acidosis2. Compensated respiratory acidosis3. Uncompensated respiratory acidosis4. Uncompensated metabolic alkalosis

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ABGs drawn from a patient in septic shock are:

pH 7.25PaC02 36HCO3

- 14

This Imbalance is MOST LIKELY:1. Uncompensated respiratory alkalosis2. Uncompensated respiratory acidosis3. Uncompensated metabolic acidosis4. Uncompensated metabolic alkalosis

A 48 year old female is receiving large doses of diuretics for persistent left ventricular failure. She is somewhat irritable this A.M. and displays tremulous activity.

Renal panel: K+ is 2.5 Cl- is 84

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pH 7.58PaC02 43HCO3

- 33B.E. +9Pa02 76

This Imbalance is MOST LIKELY:1. Compensated metabolic alkalosis2. Uncompensated respiratory acidosis3. Uncompensated metabolic acidosis4. Uncompensated metabolic alkalosis

A COPD patient has the following ABGs:

pH 7.39

PaC02 50

HCO3- 28

After analyzing this, the nurse should:1. Request another test2. Compare these results to the patients baseline3. Call the lab to verify the results4. Notify the physician stat

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QUESTIONS?

2/28/2022

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Kelly Urban, MEd, BSN, RN, CCRN-K, TCRN

Acute Respiratory Distress Syndrome (ARDS)

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Objectives• Define ARDS• Discuss treatment strategies for ARDS• Describe the steps involved in proning

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Case Scenario65 year old male admitted to hospital for shortness of breath, fever, and non-productive cough for past 2 days.(Past medical history includes hypertension and diabetes)

• Initial Vital Signs: HR 110, BP 82/42, RR 36, SPO2 88%, Temp 102.2

What should the initial treatment include?

What initial Lab/Diagnostics do we need to obtain?

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Case Scenario65 year old male admitted to hospital for shortness of breath, fever, and non-productive cough for 2 days

• Initial Vital Signs: HR 110, BP 82/42, RR 36, SPO2 88%, Temp 102.2• Initial ABG: pH 7.30, PaO2 52, PaCO2 52, HCO3 18• Other Labs:

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Overview of Respiration

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Gas Exchange

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Respiratory FailureSyndrome in which the respiratory system fails in 1 or more of its gas exchange functions

– Hypoxemia• Most common (defined as PaO2 < 60 mmHg)• Diseases of lung which involve fluid filling or collapse of alveoli

– Hypercapnia• Defined as PaCO2 > 50 (non-chronic)• Inadequate air flow (hypoventilation)

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Acute Respiratory Distress Syndrome (ARDS)• Clinical syndrome of lung injury with hypoxic respiratory failure

• Typically caused by intense pulmonary inflammation that develops following an insult

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Physiologic Effects of Inflammatory Response• SIRS response• Uncontrolled release of inflammatory

mediators• Vasodilation• ↑ microvascular permeability• Cellular activation adhesion• Coagulation

ARDS is the manifestation of SIRS within the lungs

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Risk Factors• Age• Co-morbidities• Positive Fluid Balance• Steroids (prior to onset)• Blood Transfusions• Late Intubation

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Diagnostic Procedures• History/Physical• Laboratory

– ABG• Imaging

– Chest x-ray or CT chest– Echo

Signs/Symptoms:• Tachypnea• Progressive Refractory Hypoxemia• Bilateral Pulmonary Infiltrates

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Signs & Symptoms• Tachypnea/Tachycardia at rest• Progressive refractory hypoxemia• CXR – bilateral pulmonary infiltrates• Cyanosis• Hypotension• Use of accessory muscles

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Case Scenario continued65 year old male admitted to hospital for shortness of breath, fever, and non-productive cough for 2 days. He was intubated and admitted to the ICU.

• Current Vital Signs: HR 100, BP 98/52, RR 16, Temp 100.2• Current ABG (vent CMV- 50% FiO2, PEEP 8):

– pH 7.24, PaO2 60, PaCO2 45, HCO3 20

Does this patient have ARDS?

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ARDS

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Berlin Definition – ARDSTiming Within 1 week of a known clinical insult of new/worsening respiratory

symptomsChest Imaging (x‐ray or CT)

Bilateral opacities – not fully explained by effusions, lobar/lung collapse, or nodules

Origin of Edema Respiratory failure not fully explained by cardiac failure or fluid overloadOxygenation Mild Moderate Severe

P/F Ratio 201‐300 (PEEP > 5 cmH2O)

P/F Ratio 101‐200 (PEEP > 5 cm H2O)

P/F Ratio < 100(PEEP > 5 cm H2O)

16

PaO2/FiO2 (P/F) Ratio• Relationship of amount of additional oxygen to create a specific PaO2– PaO2/FiO2

– Normal > 300ARDS Severity based on P/F Ratio:• Mild – 201‐300• Moderate – 101‐200• Severe – < 100

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17

Case Scenario continued65 year old male admitted to hospital for shortness of breath, fever, and non-productive cough for 2 days. He was intubated and admitted to the ICU.

• Current Vital Signs: HR 100, BP 98/52, RR 16, Temp 100.2• Current ABG (vent CMV- 50% FiO2, PEEP 8):

– pH 7.24, PaO2 60, PaCO2 45, HCO3 20

What is this patient’s P/F ratio?Does this patient have ARDS?

18

ARDS Characteristics• Bilateral Pulmonary Infiltrates on CXR• Non-cardiogenic Pulmonary Edema• Refractory Hypoxemia• Diffuse Alveolar Damage

19

Case Scenario continued65 year old male admitted to hospital for shortness of breath, fever, and non-productive cough for 2 days. He remains intubated and in the ICU.

• Current Vital Signs: HR 100, BP 98/52, RR 16, SpO2 90%• Current ABG (vent 50% FiO2, PEEP 8): pH 7.24, PaO2 60, PaCO2 45, HCO3 20

What is this patient‘s P/F Ratio?Does this patient have ARDS?What Treatment is needed?

20

ARDS Treatment/Management Goals• Maintain oxygenation – PaO2 55-80 mmHg or SPO2 88-95%• Avoid ventilator-induced lung damage• Maintain neutral or net-negative fluid balance in hemodynamically stable patients– CVP 4-8 mmHg– Urine Output > 0.5 ml/kg– Adequate cardiac output

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21

ARDS Treatment/Management

22

23 24

ARDS Treatment/Management• Lung Protective Ventilation (to prevent vent complications)

– Tidal Volume (4-8 ml/kg predicted body weight – typically 4-6)– Plateau Pressure < 30 cm H2O

• Non-invasive Ventilation Strategies

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25

Aerosol-Generating Procedures• Intubation• Extubation• NIPPV• HFNC• BVM• CPR• Bronchoscopy

26

Non-Invasive Oxygenation Strategies• High Flow Nasal Cannula• Proning• Inhaled vasodilators

27

High Flow Nasal Cannula (HFNC)• Provide O2 & noninvasive ventilator support

– Reduces need for intubation• Appropriate for:

– Mild to moderate acute respiratory support– Symptom control (thickened secretions, cough, dyspnea, hypoxemia)– Post-Extubation

28

HFNC

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29

HFNC• Nasal prongs – do not occlude > 50% of nares• FiO2, Temperature, & Liter Flow are Independent

– Titrate FiO2 for SPO2

– Titrate L/min for work of breathing– Set temperature to 37oC and adjust to patient preference

30

HFNC

31

HFNC Protective Measures• Surgical mask over patient’s nose/mouth

32

Proning• Shift weight from back to front• Improves pulmonary mechanics• Take off heart weight from the lungs• Improves oxygenation and mortality• Can be performed on intubated or non-intubated patients

~ 17% lung compressed ~ 4% lung compressed

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33

Proning Mechanics

34

Self-Proning (Non-intubated)• Assess patient mobility/mental status (ability to independently change position in bed)

• Monitoring equipment ECG/SPO2• HOB elevated 10-25 degrees (reverse Trendelenburg) if receiving tube feeds

• Attempted for at least 30 minutes (at least twice in 24 hour period)

35

Proning• System-based approach

– Nurses– Respiratory Therapists– Technicians– Physician

• Equipment– Pillow (2 or 3)– Sheet

AACN Procedure 19

36

Proning

• Should be used if P/F Ratio < 150 mmHg to reduce mortality (FiO2 > 0.6, PEEP > 5)

• Sessions of at least 16 consecutive hours

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37

Proning Risks• Increased need for sedation/paralysis• Increased hemodynamic instability• Transient desaturation• Accidental extubation• Accidental dislodgement of lines, tubes

38

Proning Contraindications• Spinal instability• Unstable fractures especially face / pelvis• Open wounds • Shock• Pregnancy• Tracheal surgery

39

Proning Steps

40

Proning

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41

CPR in the Proned Position(with an advanced airway in place)• Start manual compressions on the back• Place hands at T7-T10• Need solid surface• Place defibrillator pads anterior/posterior (sandwich the heart)

Prone CPR from AHA:When the patient cannot be placed in the supine position, it may be reasonable for rescuers to provide CPR with the patient in the prone position, particularly in hospitalized patients with an advanced airway in place (Class Iib, LOE C).

42

Inhaled Vasodilators• Selective vasodilation• Helpful if pulmonary HTN involved• Can improve V/Q mismatch & oxygenation• Inhibits platelet aggregation & adhesion• Some anti-inflammatory effects• No decrease in mortality rates

43

ECMO• Should be considered in cases of severe ARDS (P/F ratio < 80 mmHg)

44

Case Scenario continued65 year old male admitted to hospital for shortness of breath, fever, and non-productive cough for 2 days. He remains intubated and in the ICU. He has been proned for past 16 hours.

• Current Vital Signs: HR 88, BP 99/58, RR 20, SPO2 93%• Current ABG (vent CMV- 40% FiO2, PEEP 6):

– pH 7.35, PaO2 74, PaCO2 45, HCO3 22

What is this patient‘s P/F Ratio?Is the patient improving?

2/28/2022

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45

References• https://www.uptodate.com/contents/coronavirus-disease-2019-covid-19• https://sccm.org/SurvivingSepsisCampaign/Guidelines/COVID-19• https://www.ncbi.nlm.nih.gov/books/NBK436002/• https://annalsofintensivecare.springeropen.com/articles/10.1186/s13613-019-

0540-9• https://www.elsevier.com/__data/assets/pdf_file/0010/990721/Acute-

respiratory-distress-syndrome-in-adults-CO.pdf• https://www.ncbi.nlm.nih.gov/books/NBK526071/

46

[email protected]

2/23/2022

1

Pacemakers

Mary Jane Willard, RN

Clinical Educator

Central Arkansas Veterans Healthcare System

LRCCP Basic Critical Care Class

March 3, 2022

No conflicts of interest to disclose.

Learning Objectives

Identify the different types of pacemakers.

Recognize different rhythms associated with

pacemaker malfunction.

Describe the pacemaker codes.

PacemakersA medical device that generates

an electrical impulse to cause the

heart muscle to contract. This

process helps regulate the

electrical conduction of the heart.

PacemakersIf the patient cannot maintain

an adequate cardiac output,

use of a temporary or

permanent pacemaker may be

warranted.

Siva K. Mulpuru et al. J Am Coll Cardiol 2017; 69:189-210.2017 American College of Cardiology Foundation

Pacemaker History Pacemaker History

The first implanted pacemaker therapy was introduced in 1958 in

Stockholm. The pacemaker failed within just a few hours. The patient had

another pacemaker placed in 1960. Additionally, he had 26 more

pacemakers implanted in 43 years and outlived the surgeon that save his

life. He died in 2001 of Melanoma at the age of 86 years old.

Jeffrey, K., & Parsonnet, V. (1998). Cardiac pacing, 1960–1985: a quarter century of medical and industrial innovation. Circulation, 97(19), 1978-1991.

Coombes, D. (2021). Pacemaker therapy 1: clinical indications, placement and complications. Nursing Times, 117, 11-22.

Photograph: https://en.wikipedia.org/wiki/Arne_Larsson_(patient)

1 2

3 4

5 6

https://en.wikipedia.org/wiki/Arne_Larsson_(patient)

2/23/2022

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The First Pacemaker Implanted into a Patient EKG before pacemaker

Larsson, B., Elmqvist, H., Ryden, L., & Schüller, H. (2003). Lessons from the first patient with an implanted pacemaker: 1958–

2001. Pacing and Clinical Electrophysiology, 26(1p1), 114-124.

EKG after pacemaker (Oct 8, 1958)



EKG after pacemaker (Oct 15, 1958)



1960 Veterans Administration Pacemaker

Aquilina O. A brief history of cardiac

pacing. Images Paediatr Cardiol. 2006;8(2):17-81.

American Journal of Cardiology 2010 106810-

818DOI: (10.1016/j.amjcard.2010.04.043)

On June 6, 1960, two years later the VA in Buffalo, NY carried out the first

successful implantation of a battery-powered pacemaker with myocardial lead. The

77-year-old Veteran lived for 18 months after the surgery. There were 15 more

Veterans with complete heart block that received a pacemaker that year.

In 1972, the first lithium battery was introduced.

Modes of Pacing1. Fixed rate (asynchronous): Impulses are

delivered at a predetermined rate.

2. Demand (synchronous): Impulses are

delivered at a predetermine rate ONLY IF

the patient’s own heart rate is less than

the pacemaker’s set rate.

7 8

9 10

11 12

2/23/2022

3

Pacemakers• A mechanical device to stimulate the heart to

contract

• Indications for Pacing:– Temporary

• After heart surgery

• Medication intoxication such as digoxin

• Bridge to permanent pacing

• Failure of permanent system

• Overdrive pacing of tachycardia

• Acute MI with CHJB or Mobitz II

– Permanent• Congenital heart blocks

• Acquired heart block (most often secondary to degeneration of the conduction system)

• Sick Sinus Syndrome (SSS)

– Brady-tachy Syndrome

– Tachy-brady Syndrome

Pacemakers• Methods of pacing

– Temporary (generator external to the body)

• Transvenous - through a vein

• Epicardial – wires on epicardial surface of the heart

• Transcutaneous – through electrodes placed on the chest wall

– Permanent

• All components of the system are inside the body

Pacemakers• Components

– Pulse Generator – also called battery.

• Contains battery (power source) and “brains” of system

– Wire – Connects pulse generator to the electrode

– Electrode – That part of system in contact with the heart

muscle that transmits impulse and can detect electrical

activity of heart.

Location of Pacemaker Leads• Temporary Pacing

– Transcutaneous: anterior and posterior of chest

– Transvenous: right ventricle

– Epicardial: right atrium and/or right ventricle

• Permanent Pacing

– Right ventricle

– Right atrium

– Both right ventricle and right atrium

– Bi-ventricular – right ventricle & coronary sinus

• Usually implanted in Cardiac Cath Lab

Permanent Generator Pacemaker Terminology

• Single chamber pacing: Only one lead in the

heart; only one chamber being paced such as

the right atrium or right ventricle.

• Pacing the right atrium is called

– Atrial pacing

• Pacing the right ventricle is called

– Ventricular pacing

13 14

15 16

17 18

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Single Chamber pacemaker SINGLE PACEMAKER SPIKES

Queen’s School of Medicine

Pacemaker Terminology

• Dual chamber pacing: Two leads in the heart;

one or both chambers being paced such as

the right atrium or right ventricle

• Pacing the right atrium is called

– Atrial pacing

• Pacing the right ventricle is called

– Ventricular pacing

• Pacing of both atrium and ventricle

– A-V sequential pacing

Dual Chamber pacemaker

DOUBLE PACEMAKER SPIKES

Queen’s School of MedicineWWW.MEDTRONICACADEMY.COM

19 20

21 22

23 24

http://www.medtronicacademy.com/

2/23/2022

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Pacemaker Terminology

• Bi-ventricular pacing: Two leads in the heart; one or both

chambers being paced such as the right atrium or right

ventricle

• Both ventricles and atria are paced

– Of benefit to the Heart Failure patient who has

dyssynchrony of the left and right ventricles

Biventricular Pacemaker

www.medtronicacademy.com

Temporary Pacemakers

Transcutaneous

Epicardial

Transvenous

Generator

Leads

Patches

Equipment needed for

temporary pacing:

30

Transcutaneous Pacing

25 26

27 28

29 30


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31 32

Transcutaneous

Pacing

Sternum-apex pacing electrode placement. In female patients, position the negative pacing electrode under the breast but above the diaphragm to prevent contraction of the diaphragm each time the pacer fires. (Modified from illustrations supplied by Physio-Control, Inc., Redmond, WA.)

33 34

Temporary Generator

(Transvenous or Epicardial)

Single Chamber or Dual Chambers

www.Medtronicacademy.com

Pacer cables

Disposable Non-disposable

36

31 32

33 34

35 36


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Epicardial Wires

Anatomy of the temporary pacemaker circuit, Alex Yartsev

Epicardial Wires

WWW.MEDTRONICACADEMY.COM

Transvenous

PacingTransvenous wires

41

Universal Pacemaker Code

• A universal means of identifying the numerous functions of pacemakers by using a series of letters that represent a function.

• Need to know the first three positions (there are 5 or more).

• The code tells you the basic functioning of the generator.

• Not knowing how a pacemaker is programmed could result in misinterpretation of the rhythm.


37 38

39 40

41 42



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43


• Letters used in the code:

– A = Atrium D= Dual (A + V)

– V= Ventricle O = None

– I = Inhibited T = Triggered

• First three positions

– Chamber paced

– Chamber sensed

– Response to a sensed event

44


• Examples of Code– V V I:

• First letter V = Ventricular pacing

• Second letter V = Ventricular sensing

• Third letter I = Ventricular output inhibited if intrinsic event sensed

– DDD:

• First letter D = A + V paced

• Second letter D = A + V sensed

• Third letter D = T and I response to sensed event

45


• Other examples include:

– V O O

– A A I

• Letters 4 and 5 of code indicate such functions as:

– Multiprogrammability

– Rate responsiveness

– Communication possibilities

46

ECG Recognition of A Pacemaker Rhythm

• When the pacemaker “fires” or

stimulates the heart to contract, an

electronic spike is seen on the ECG.

• This “spike” is a vertical line either

above, below or both the baseline.

• After the “spike” there will be a

waveform which tells you which

chamber was stimulated: a P wave or a

QRS complex.

47

Pacemaker Identification

• Example of a Pacemaker Rhythm

• Note the “spike” preceding each complex

48

Pacemaker Identification• After each pacemaker spike there

should be evidence the heart

depolarized. Either a P wave

(depolarization of the atria) or a QRS

complex (depolarization of the

ventricles).

• Atrial Pacing: spike followed by a P

wave

• Ventricular Pacing: spike followed by a

QRS complex

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45 46

47 48

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49

A Pacemaker Rhythm

• Pacemaker stimulus seen as a vertical spike

• Spike will precede the response of the heart

50

Terms used in the Interpretation of

Pacemaker Rhythm

• Capture: pacemaker spike is followed by

evidence of depolarization of the heart

– Normal is “complete capture”

• Sensing: pacemaker detects intrinsic cardiac

beats

– Appropriate

– Inappropriate: doesn’t sense

• Oversensing

• Undersensing

• Rate: rate at which the pacemaker is firing

51

Interpreting a Pacemaker Rhythm

• Look for the “spike”

• Does spike precede a P wave or a QRS complex?

• Measure rate of pacemaker– Measure from spike to spike

• Is there appropriate function? Firing, Capture, Sensing

• Interpretation: Ventricular Pacing, rate with complete capture; Comment on sensing if sensing can be evaluated.

52

Pacemaker Malfunction

• Failure to Capture

– Capture is the successful depolarization of the

heart by the pacemaker

– Capture is recognized by a pacer spike which is

followed by the appropriate wave form

• P wave if atrial pacing

• QRS if ventricular pacing

– Failure to capture (loss of capture) recognized as

pacer spikes not followed by a waveform

Berberian JG. EMRA EKG Guide. 1st ed. Dallas, TX: Emergency Medicine Residents’ Association; 2017.

53


• Failure to Sense (Undersensing)– Pacemaker spikes appear on the ECG when they

should not; generator has failed to recognize intrinsic cardiac activity

Berberian JG. EMRA EKG Guide. 1st ed. Dallas, TX: Emergency Medicine Residents’ Association; 2017.54

Pacemaker Malfunction • Failure to Sense

(Undersensing)

– Pacemaker spikes appear on the ECG when they should not; generator has failed to recognize intrinsic cardiac activity

Rounds, A. (2014). An uncommon cause of pacemaker-mediated ventricular tachycardia. Journal of cardiovascular

electrophysiology, 25(1), 107-109.

49 50

51 52

53 54

https://www.amazon.com/EMRA-EKG-Guide-Jeremy-Berberian/dp/1929854498/


2/23/2022

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55


• Failure to Sense (Oversensing)– Results from generator sensing extraneous electrical

signals (EMI) or misidentifies a T wave or P wave for the QRS and does not emit a stimulus.

– Recognized by the absence of pacer spikes or pacing at a slower rate than preset interval. Can result in failure to fire….no pacer spikes seen.

56

Pacemaker Malfunction• Failure to Fire

– Pacemaker fails to deliver an electrical stimulus or when it fails to deliver the correct number of stimuli per minute.

– Recognized on ECG as absence of pacemaker spikeswhen they should be present

– May result in bradycardia, syncope, chest pain, hypotension

– Causes include battery depletion, electrode displacement, lead fracture, increased impedance, sensing problems

Berberian JG. EMRA EKG Guide. 1st ed. Dallas, TX: Emergency Medicine Residents’ Association; 2017.

57

Pacemaker Rhythms

• Ventricular Pacing

– Rate: 86 with intermittent loss of capture (pacer spikes not followed by a

waveform)

– Treatment: Report to MD Immediately; continue to monitor; anticipate

TCP

58

Pacemaker Rhythms

• Ventricular Pacing: Rate: ? with inappropriate sensing

– Note pacemaker spikes in the QRS complexes)

• Treatment: Report Immediately to MD

59

Pacemaker Rhythms

• Situation: Lower Rate Limit of Ventricular Pacer: 62 bpm

• SR rate 79 with SNF (3.52 sec pause) with failure to fire

• Treatment: Report to MD immediately; anticipate TCP

60

Complications

• Temporary

– Pain

– Tissue damage if defibrillated

– Failure to correctly ID pacer malfunction

– Infection, bleeding

– Pneumothorax

– Perforation of ventricle

– Instability of the system

55 56

57 58

59 60


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61

Complications

• Permanent Pacing– Bleeding, Infection

– Thrombosis at lead interface with heart

– Electrode displacement, Lead fracture

– Perforation of ventricle

– Pacemaker Syndrome

– Changes in impedance of lead

– Battery depletion (life is 10 – 11 years with lithium battery)

62

Implantation

• Temporary

– At bedside: transvenous, transcutaneous

– Cardiac Cath Lab (CCL): transvenous

– In surgery: epicardial

• Permanent

– CCL

– Surgery

63

Implantation

• Temporary

– Local anesthesia

– Battery external to body

• Permanent

– Local/IVCS

– Battery placed in pocket created beneath

clavicle – R or L

64

Pacemakers

• Permanent

– Subclavian vein to heart – RA

&/or RV to position lead(s)

– Pulse Generator positioned in a

sub-clavicular pocket

65

Temporary

– Monitor site

– Frequent checking of connections

– Restriction of movement may be necessary

– Electrical precautions to prevent micro-shock

– Monitor ECG for appropriate pacer function

– Monitor patient response to pacing

66

Post-Implant

• Permanent– Initial period of bedrest (24 hrs) to allow lead to “settle in”

– Initial restriction of movement of shoulder; wear sling; avoid heavy lifting; over head use of involved arm

– Monitor site for hematoma, bleeding, infection

– Monitor ECG for appropriate pacer function

– Patient Teaching: follow-up; interference; ID card; Medic-Alert tag

61 62

63 64

65 66

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67

Post-Implant

• Follow-up: Check magnet rate; A decrease of 2

bpm indicates need for battery change

• Patient goes into VF and cardiac arrest.

– Begin CPR; defibrillate as soon as defib

available

– Avoid placing electrodes/paddles over and/or

near generator (hands-width away)

– Pacemaker may malfunction post shock

68

Pacemaker Rhythms

Atrial Pacing

Ventricular Pacing

69

Pacemaker Rhythms

• Atrial Pacing

– Rate: 58 with Complete Capture

– Treatment: none; continue to monitor

– Note: can’t evaluate sensing-no intrinsic beats seen

70

Pacemaker Rhythms

• Interpretation: Ventricular Pacemaker

– Rate: 79 with Complete Capture and appropriate sensing

– Treatment: None; continue to monitor

71

Pacemaker Rhythms• A-V Sequential Pacing (both atrial and ventricular spikes seen)

– Rate: A = 56, V = 56

– Complete Capture

– Treatment: none; continue to monitor

72

Pacemaker Rhythms

• Interpretation:

– A - V Sequential Pacing Rate: 63 with complete capture

• Treatment: none; continue to monitor

67 68

69 70

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73

Pacer Malfunction

• Failure to Capture

– Lead displacement or fracture

– Sensing problems

– Battery depletion

WWW.MEDTRONICACADEMY.COM




73 74

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77 78





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ATRIAL ELECTROGRAM

Indications:

• When atrial activity id not clearly visible on the ECG.

• Trying to determine the relationship between the

atrial and ventricular activity.

• Differentiate wide-complex rhythms (Vtach vs SVT)/

• Differentiate Narrow-complex SVT (Sinus Tach/Atrial

Tach, PSVT, A Flutter, A Fib, Junctional Tach)

http://booksite.elsevier.com/9780323376624.

Atrial Electrocardiogram

• Take V lead with

electrode and place

over end of epicardial

wire

• Then print out a strip

with a limb lead and

the V lead

simultaneously

• Helpful with diagnosis

of rhythm origin -

atrial vs. junctional or

ventricular

Atrial ECG

References• Alspach, J. (2006). AACN core curriculum for critical care nursing.Aquilina O. A brief history of

cardiac pacing. Images Paediatr Cardiol. 2006;8(2):17-81.

• Berberian JG. EMRA EKG Guide. 1st ed. Dallas, TX: Emergency Medicine Residents’ Association; 2017.

• Coombes, D. (2021). Pacemaker therapy 1: clinical indications, placement and complications. Nursing Times, 117, 11-22.

• www.medtronicacademy.com

• Jeffrey, K., & Parsonnet, V. (1998). Cardiac pacing, 1960–1985: a quarter century of medical and industrial innovation. Circulation, 97(19), 1978-1991.

• https://medmovie.com/library_id/7556/topic/cvml_0076a/summary/

• Larsson, B., Elmqvist, H., Ryden, L., & Schüller, H. (2003). Lessons from the first patient with

an implanted pacemaker: 1958–2001. Pacing and Clinical Electrophysiology, 26(1p1), 114-124

• https://ecgwaves.com/topic/assessment-of-pacemaker-malfunction-using-ecg/

• Rounds, A. (2014). An uncommon cause of pacemaker-mediated ventricular tachycardia. Journal of

cardiovascular electrophysiology, 25(1), 107-109.

• Sternum-apex pacing electrode placement. In female patients, position the negative pacing electrode under the breast but above the diaphragm to prevent contraction of the diaphragm each time the pacer fires. (Modified from illustrations supplied by Physio-Control, Inc., Redmond, WA.)

• Wesley: Huszar - Basic Dysrhythmias: Interpretation & Management, 4th ed., Copyright ©

2011

79 80

81 82

83 84

http://booksite.elsevier.com/9780323376624



https://medmovie.com/library_id/7556/topic/cvml_0076a/summary/

https://ecgwaves.com/topic/assessment-of-pacemaker-malfunction-using-ecg/

3/5/2021

1

HemodynamicsRichard Milam RN, BSN, CCRN

Advanced Practice Partner

H4 Trauma/Surgical/Cardiovascular ICU, E4 Neuro/Medical ICU

University of Arkansas for Medical Sciences

Hemodynamics

Hemodynamic Parameters Normal Values Mean Arterial Pressure- MAP: 70-90 mmHg

Right Arterial Pressure- RAP: 2-6 mmHg

Central Venous Pressure- CVP: 2-8 mmHg

Cardiac Output- CO: 4-8 L/min

Cardiac Index CI: 2.5-4 L/min

Stroke Volume SV: 60-120 ml

Stroke Volume Index SVI: 33-50 ml/m2

Stroke Volume Variation SVV: 6-12%

Systemic Vascular Resistance SVR: 800-1200 dynes

SVR Index SVRI: 2000-2400 dynes

3/5/2021

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Hemodynamics

Hemodynamic Parameters Normal Values Pulmonary Artery Systolic Pressure PAS: 20-30 mmHg

Pulmonary Artery Diastolic Pressure PAD: 6-12 mmHg

Pulmonary Artery Mean Pressure PAM: 10-15 mmHg

Pulmonary Artery Wedge Pressure PAWP: 8-12 mmHg

Pulmonary Vascular Resistance PVR: 150-300 dynes

PVR Index PVRI: 225-314

Noninvasive Hemodynamic Monitoring

Noninvasive Blood Pressure

Heart Rate

Pulses

Mental Status

Skin Temperature

Capillary Refill

Urine Output

3/5/2021

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How’s the patient doing?

Blood Pressure

3/5/2021

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MAP

MAP = (SBP + (DBP x 2)) / 3

Diastole counts twice as much as systole because 2/3 of the cardiac cycle is spent in diastole.

So in a normal BP of 120/80, the MAP would = (120 + (80 x 2)) / 3 = 93.3

Most of the time we aim for a goal MAP of 60 to 65.

Shock Index

The shock index (SI) is a bedside assessment defined as heart rate divided by systolic blood pressure, with a normal range of 0.5 to 0.7 in healthy adults.

SI > 0.7 were found to have a significantly higher mortality rate.

The degree of shock was found to correlate with increasing SI value. The need for blood products, fluids and vasopressors was also found to increase with higher SI values.

3/5/2021

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Invasive Hemodynamic Monitoring

Arterial Blood Pressure

Central Venous Pressure

Pulmonary Artery Pressure

Pressure System Set-Up

Pressure Bag

Fluids

Pressure Transducer

3/5/2021

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Phlebostatic Axis

4th Intercostal space, mid-axillary line

Level of the atria

Referencing the “zeroing” stopcock to Phlebostatic Axis

The phlebostatic axis is the approximate level of the left atrium. It is located

midway between the anterior-posterior chest wall at the 4th intercostal space.

The patient need not be flat, but must be supine.

3/5/2021

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Accuracy

Zeroing transducer system to negate atmospheric pressure Open air-reference port on transducer

Push appropriate “button” on bedside monitor

Calibration to avoid electronic drift Rechecked q shift

Maintaining continuous flush Fluid in flush bag

Pressure bag at 300 mmHg

All readings are taken at end of expiration

CVP The CVP catheter is an important tool used to assess right ventricular function and

systemic fluid status.

Normal CVP is 2-8 mm Hg.

CVP is elevated by :

overhydration which increases venous return

heart failure or PA stenosis which limit venous outflow and lead to venous congestion

positive pressure breathing, straining,

CVP decreases with:

hypovolemic shock from hemorrhage, fluid shift, dehydration

negative pressure breathing which occurs when the patient demonstrates retractions or mechanical negative pressure which is sometimes used for high spinal cord injuries.

The CVP catheter is also an important treatment tool which allows for:

Rapid infusion

Infusion of hypertonic solutions and medications that could damage veins

Serial venous blood assessment

3/5/2021

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CVP

Arterial Line An arterial line (also art-line or a-line) is a thin catheter inserted into

an artery. It is most commonly used in intensive care medicine and anesthesia to monitor blood pressure directly and in real-time (rather than by intermittent and indirect measurement) and to obtain samples for arterial blood gas analysis.

An arterial line is usually inserted into the radial artery in the wrist, but can also be inserted into the brachial artery at the elbow, into the femoral artery in the groin, into the dorsalis pedis artery in the foot, or into the unlar artery in the wrist. A golden rule is that there has to be collateral circulation to the area affected by the chosen artery, so that peripheral circulation is maintained by another artery even if circulation is disturbed in the cannulated artery.

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Arterial Line Indications

Closely Monitor Blood Pressure

Vasoactive drips (dopamine, nipride, etc)

Frequent B/P measurements are needed

Frequent blood sampling indicated

Cardiac Output and other hemodynamic measurements. (Vigileo/Flotrac)

A-line Waveforms

A-line pressure waveform represents the ejection phase of left-ventricular systole

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Components of Arterial Waveform

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The Square Wave Test: 1.5 – 2 Oscillations

Overdampened: < 1.5 oscillations

Results in erroneously low SBP and high DBP

Causes:

large air bubbles

Loose/open connections

Low fluid level in flush bag

Pressure bag less than

300 mmHg

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Underdampened: > 2 oscillations

Results in erroneously high SBP and low DBP

Causes:

Small air bubbles

Tubing too long

Defective transducer

Understanding Hemodynamics

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Cardiac Output

Preload

Preload- the amount of myocardial stretch at the end of diastole/filling after a contraction. (Volume)

Concept

Stro

ke V

olum

e

End-diastolic Volume

A

B C

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Preload Terminology

Stroke Volume:

Difference between the end-diastolic volume (amount of blood in the ventricle at the end of diastole) and end-systolic volume (blood volume in the ventricle at the end of systole)

Normal SV: 60 – 100 ml

Ejection Fraction:

Stroke Volume expressed as a percentage of end-diastolic volume.

Normal EF: 60-75%

Preload

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Preload Parameters

SV= Stroke Volume

The amount of blood pumped by the left ventricle of the heart in one contraction.

Normal: 60-100 ml/beat

SVI= Stroke Volume Index

Normal: 30-50 ml/beat/m2

SVV= Stroke Volume Variation

Normal= <13

Stroke Volume Variation is Pulsus Paradoxus

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Limitations of SVV Mechanical Ventilation

Currently, literature supports the use of SVV on patients that are 100% mechanically (control mode) ventilated with tidal volumes ≥ 8cc/kg and fixed respiratory rates.

Spontaneous Breathing

Unless taking regular rate, and adequate tidal volumes…

Arrhythmias

Previously, arrhythmias dramatically affected SVV. However, early 2012 software upgrade able to filter out arrhythmias

(6 PVCs per 20 sec)

Preload can be affected by

Anything that changes circulating blood volume (dehydration, hemorrhage, hypervolemia, etc)

Anything that changes the amount of blood returning to the heart (vasoconstriction, vasodilation, etc)

Anything that changes the ventricular filling time or volume (Heart Failure, cardiac tamponade, or heart rate)

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Decreased Preload

If preload is too low, causes include: dehydration, hemorrhage, hypovolemia, vasodilation, tachycardia (decreased filling time)

Symptoms include:

Tachycardia Cool, clammy skin

Decreased UO Decreased BP

Chest Pain Dizziness

Treatment for Preload

Fluids (most common)

Tx to slow heart rate and increase filling time

For SVT or VT

Vasoconstrictor (nor-epi, epi drips) If and only if the tank is full

Vasodilation due to

sepsis/ anaphylaxis, etc

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PLR or Passive Leg Raise

Fluid Challenge

Fundamentally, the only reason to give a patient a fluid challenge is to increase SV. As preload increases, left ventricular SV increases until optimal preload is achieved, at which point SV remains relatively constant.32

Measure SV

Deliver fluid (200 - 250mL)

SV increase > 10% ?

YES

NO

Monitor SV for clinical signs of fluid loss

SV change < 10% ? YES

NO

Initiate Bundle

Preload- Stroke Volume

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Not measuring Stroke Volume?

Look at pulse pressure

Systolic – diastolic = Pulse Pressure

Normal is 30-40 mm Hg

↑ in Pulse Pressure = ↑ in stroke volume

Increased Preload

Possible Causes

Fluid overload

Hypervolemia

Vasoconstriction

Heart failure

Possibly bradycardia, exercise

Signs/Symptoms:

CVP > 8

Decreased CO

Dist. Neck Veins

Hepatojugular Reflux

Weight gain

Peripheral edema

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Treatment of Left Preload

Diuretic to circulating volume

Medication to vasodilate to trap circulating volume in the periphery (NTG)

Positive Inotrope: increase strength of contraction (dobutamine)

Stop negative Inotropes (stop Ca++ Channel blocker, Beta Blockers, etc)

Afterload

Afterload has an inverse relationship to ventricular function

As resistance ↑, the force of contraction ↓ = ↓stroke volume.

As resistance ↑, myocardial oxygen consumption ↑

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Afterload

Tension developed by the myocardial muscle fibers during ventricular systolic ejection

Described as resistance, impedance, or pressure that the ventricle must overcome to eject its blood volume

Systemic Vascular Resistance (SVR)

Most sensitive measure of afterload for the left ventricle

Normal: 800-1200 dynes

Pulmonary Vascular Resistance (PVR)

Most sensitive measure of afterload for the right ventricle


SVR & PVR

SVR = Left Ventricular Afterload

MAP – CVP x 80

CO

PVR = Right Ventricular Afterload

MPAP – PAWP x 80

CO

MAP: Mean Arterial Pressure

MPAP: Mean Pulmonary Artery Pressure

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Afterload Affected By

Anything that or vascular resistance

Vasoconstriction, vasodilation, IABP

Anything that affects

the aortic valve or aorta on the left

Aortic stenosis

Aneurysm

Miss-timed IABP Pulmonic valve or pulmonary artery on the right

Afterload

High – vasoconstriction Hypertension

Vasopressors

Aortic Stenosis

Hypothermia

Pulmonary Hypertension

Hypoxia

PE

Pulmonary Stenosis

Low - Vasodilation Distributive Shock states

Vasodilators

IABP

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Right Ventricular Afterload (PVR)

High Pulmonary Embolism

Pulmonary hypertension

Left ventricular failure

Low Lysis of Pulmonary Embolism

Treatment of PVR

Left Ventricular Afterload (SVR)

High Vasoconstriction

Vasopressors

Hypertension

Compensatory mechanism for CO states (hypovolemia/cardiogenic shock)

Aortic Valve Stenosis/ aortic aneurysm

Miss-timed IABP

Low Vasodilation

Nipride /NTG drips

Distributive Shock StatesAnaphylaxis

Sepsis

Neurogenic

Intra-Aortic Balloon Pump

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Treatment of High Afterload

Medication to vasodilate

Surgery to correct aortic stenosis/ aneurysm

is due to CO, treatment is aimed at

CO (positive inotrope, etc)

Treatment of Low Afterload

Medications for vasoconstriction

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Contractility

Inotropic state of the myocardium

The velocity and extent of myocardial fiber shortening

Parameters that reflect contractility include

Stroke Volume

Stroke Volume Index

Left ventricular stroke work index

Right ventricular stroke work index

Contractility

Pumping ability of the heart

Estimated by Stroke Volume/Ejection Fraction

SV = 60-130 ml

SV = CO ÷ HR

Ejection Fraction:

Stroke Volume expressed as a percentage of end-diastolic volume.

Normal EF: 60-75%

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ContractilityHigh

Positive inotropic drugs

Dobutamine

Dopamine

Digoxin

Calcium

Increased preload

The greater the muscle stretch, the greater the contraction, up to a point: Frank-Starling Law

LOW

Negative inotropic drugs

Ca++ Channel Blockers

Beta Blockers

Acid/base imbalance

Hypoxemia

Electrolyte imbalance

Signs & Symptoms

Too much contractility: chest pain, tachycardia

Too little: Heart Failure, Pulmonary Edema, decreased perfusion

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Pulmonary Artery Pressure Monitoring

Provides information about vascular capacity, blood volume, pump effectiveness, and tissue perfusion

Pulmonary Artery Catheter Components

Distal (PA) Port

Balloon Gate Valve

VIP – Venous Infusion Port

Proximal (CVP) Port

Thermistor Connector

Thermal Filament Connector

SvO2 Connector (connects to the SvO2 Optics Module)

Connects to the Cardiac Output Cable

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Indications for PA catheter use

• Intra-abdominal hypertension

• Patients at risk for acute right ventricular dysfunction

• ARDS

• Extensive burns

• Cardiac surgery

• Significant cardiac tamponade

• Significant cardiomyopathy

• Significant constrictive pericarditis

• Drug intoxication

• Severe eclampsia

• Significant intra- or extra-vascular fluid shifts

• At risk for hemorrhage

• Intra- and post-op high risk surgery management

• Patient on intra-aortic balloon counterpulsation

• Complex liver resections

• Liver transplantation

• Complex lung resection

• Complex myocardial infarctions

• Pulmonary edema

• Pulmonary hypertension

• Acute renal failure

• Severe sepsis

• Presence of or at risk for: cardiogenic, distributive, hemorrhagic, or obstructive shock

• Shock of unknown etiology

• Shock unresponsive to attempts at resuscitation

• Severe trauma

• Ventilator effects on hemodynamics

Relative Contraindications for PA catheter use Left bundle branch block

Patients with tricuspid or pulmonic heart valve replacements

Lack of appropriate clinical skills or infrastructure to insert and/or support the use of a pulmonary artery catheter

Heparin coated catheters in patients with known sensitivity to heparin (HIT) -Ensure catheter is Heparin-free for such patients

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Preparation for Insertion of Pulmonary Artery Catheter

Catheter advancement to the pulmonary artery should be rapid, since prolonged manipulation can result in loss of catheter stiffness

Common sites for percutaneous approach include:

Internal jugular

Subclavian vein

Femoral vein

Pulmonary Artery Pressure Monitoring

Normal Readings

CVP

2-6 mmHg (or 3-8 cm H2O)

PAP

Systolic 20-30 mmHg

Diastolic 10-20 mmHg

Mean 10-15 mmHg

PAWP

6-15 mmHg (should be 2-5 mmHg less than PA diastolic pressures)

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Insertion of Pulmonary Artery Catheter: Right Atrium

The first chamber reached is the right atrium

Pressures are usually low and will produce 2 small upright waves.

CVP: 2-8 mmHg

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Pulmonary Artery Catheter Right AtriumPressures AKA CVP = Preload

Decreased RAP/CVP Pressure is < 2 mmHg

Causes are dehydration, hemorrhage, hypovolemia, vasodilation, tachycardia (decreased filling time)

Treatments are fluids (most common), slow heart rate and increase filling time (for SVT/VT), vasoconstrictor (Levo/Epi/Vaso gtts) only after tank is full

Increased RAP/CVP Pressure is > 8 mmHg

Causes are fluid overload/hypervolemia, vasoconstriction, heart failure, pulmonary hypertension, Tricuspid Valve Dysfunction and possibly bradycardia, exercise

Treatments are diuretic to circulating volume, vasodilators to trap circulating volume in the periphery (NTG), positive Inotrope to increase strength of contractions (Dobutamine/Milrinone/Digoxin), and stop negative Inotropes ( Ca++ Channel blockers, Beta Blockers)

Insertion of Pulmonary Artery Catheter:Right Ventricle

Right Ventricle: Systolic 20-28 mmHgDiastolic 0-5 mmHgMean 2-8 mmHg

The next chamber is the right ventricle

Waveforms show taller, sharp uprises and low diastolic dips

Special attention must be paid to the ECG once the catheter passes through the tricuspid valve

Ventricular ectopy may occur

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Pulmonary Artery Catheter Right VentriclePressures – Primarily RVSP & RVEF

Right Ventricle: Systolic 20-28 mmHgDiastolic 0-5 mmHgMean 2-8 mmHg

Increase RVSP Pressure is > 35 mmHg

Causes are primary pulmonary hypertension, left sided heart failure due to mitral regurgitation, aortic stenosis, congestive heart failure, PE and pulmonary fibrosis.

Primary pulmonary hypertension has no cured, treatment aimed at helping improve symptoms and slow the progress. In secondary pulmonary hypertension treatment is typically aimed at the underlying cause.

Right Ventricular Ejection Fraction is lower than Left Ventricular Ejection Fraction

Normal LVEF is 60% -75% while normal RVEF is only 43%-65%.

Meaning the right ventricle has higher enddiasolic & endsystolic volumes

Insertion of Pulmonary Artery Catheter:Pulmonary Artery

Pulmonary Artery:Systolic 20-28 mmHgDiastolic 8-12 mmHgMean 8-15 mmHg

As the catheter floats into the pulmonary artery, characteristic waveforms can again be noted

There is a rise in pressure in the pulmonary artery, especially diastole

A dicrotic notch should be visible due to closure of the pulmonic valve

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Pulmonary Artery Catheter - Pulmonary Artery Pressures – PVR, & PASP


Pulmonary Vascular Resistance (PVR)

Most sensitive measure of afterload for the right ventricle


Pulmonary Artery Systolic Pressure > 35 mmHg indicates pulmonary hypertension.

Pulmonary Artery Catheter - Pulmonary Artery Pressures – PAMP


Pulmonary Artery Mean Pressure > 25 mmHg indicates pulmonary hypertension.

Causes are primary pulmonary hypertension, left sided heart failure due to mitral regurgitation, aortic stenosis, congestive heart failure, PE and pulmonary fibrosis.

Primary pulmonary hypertension has no cured, treatment aimed at helping improve symptoms and slow the progress. In secondary pulmonary hypertension treatment is typically aimed at the underlying cause.

Remember either Quarters over Dimes = 25/10 or Rule of 8s = 28/8

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Pulmonary Artery Catheter - Pulmonary Artery Pressures – PADP


Pulmonary artery diastolic pressure is a reasonable surrogate for PAOP.

PADP is usually within about 2-5 mmHg of PAOP

PADP will be more than 5 mmHg different if the patient is tachycardic or there is a condition which increases pulmonary vascular resistance

The PADP is usually higher than the PAWP.

The diastolic pressure in the pulmonary arteries is higher because of the resistance to flow in the pulmonary arterial network.

So if the flow eliminated (by occluding the artery) the pressure drops.

Insertion of Pulmonary Artery Catheter:Wedge

PAWP: 8-15 mmHg

The catheter (with the balloon still inflated) is now advanced further until it finally wedges in a central branch of the pulmonary artery.

Waveform seen is a reflection of the left atrium

The waveform will have 2 small rounded excusions from left atrial systole and diastole

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Pulmonary Artery Catheter - Pulmonary Artery Occlusion Pressure AKA Wedge Pressure

PAWP: 8-15 mmHg

PAOP: Left Ventricular Filling Pressure reflects Volume , Ventricular Compliance , & Valve Integrity (Mitral)

Elevated PAOP reflects an increase of LV end-diastolic pressure due to LV diastolic and/or systolic dysfunction/failure. PAOP less than 18 mmHg, if measured, supports criteria for the definition of acute respiratory distress syndrome and acute lung injury.

Pulmonary Artery Catheter - Pulmonary Artery Occlusion Pressure AKA Wedge Pressure

PAWP: 8-15 mmHg

Under normal conditions, when there is no diastolic dysfunction and pericardial pressures are low, PAOP correlates well with LV preload.

However with either pericardial constraint or positive pressure ventilation and PEEP, a disparity occurs between the changes in intracavitary LVEDP and those in transmural LVEDP.

So when a patient receives positive pressure ventilation with PEEP, PAOP increases and cardiac output decreases.

This decrease in CO can be reversed with volume expansion to bring preload to pre-PEEP levels.

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Caring for the patient with a PA catheter

Read pressures at the end of expiration (intrathoracic pressure changes from breathing, mechanical ventilation, or PEEP/PS will alter PAP and PAWP)

Keep in mind that right ventricular pressure readings are obtained only during catheter insertion

Normal:

Systolic: 20-30 mmHg

Diastolic: 0-5 mmHg

Mean: 2-8 mmHg

Level the transducer with the phlebostatic axis

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The other half of the Pie – SvO2 & ScVO2Normal: SvO2 - 60%-80% & ScvO2 - 70%

SvO2 = mixed venous saturation of oxygen. It is the % of oxygen remaining in the venous blood returning to the right side of the heart. This is the oxygen left over in the blood after supplying all the parts of the body except the head.

ScvO2 = central venous oxygen saturation. It is the oxygen saturation of venous blood coming from the head and upper body. It is measured from the superior vena cava, that drains blood from the head and upper body.

SvO2 requires a Swan Ganz while a ScvO2 only requires a CVL.

The procedure for assessing Scvo2 is less risky and has far lesser complications than measuring Svo2.


Maintaining the balance between oxygen delivery (DO2) and consumption (VO2) to the tissues is essential for cellular homeostasis and preventing tissue hypoxia and subsequent organ failure.

Significantly elevated levels (>80%) may indicate: Inability to use oxygen delivered to the tissues (sepsis), significantly high cardiac output, shunting of oxygenated blood past tissue or technical errors.

Significantly low oximetry levels (<60%) readings usually indicate either low oxygen delivery (DO2) or an increase in consumption (VO2) from:

Low cardiac output, low hemoglobin, low arterial oxygen saturation (SaO2)

Or increased oxygen consumption/metabolic demand from fever, pain, anxiety, shivering, seizures, burns, and work of breathing.

The first three (above) are indicators of DO2, while the fourth is an indicator of VO2.

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Blood Pressure

76

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Compensatory Mechanisms

Static vs Dynamic Parameters

Static Parameters- single snapshots

Dynamic Parameters- Trends

78

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MAP and Volume Loss

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• Healthy subjects tolerate a 25–30% decrease in blood volume without changes in systemic arterial pressure or heart rate.

• Splanchnic perfusion is compromised after 10–15% reduction in intravascular volume.

Hamilton-Davies C, Mythen MG, Salmon JB, Jacobson D, Shukla A, Webb AR. Comparison of commonly used clinical indicators of hypovolaemia with gastrointestinal tonometry. Intensive Care Med 1997; 23: 276–81

Shock - Defined

Inadequate tissue perfusion

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Stages of Shock

Compensated Tachycardia, “Normal BP” with narrowed pulse pressure, Tachypnea, ↓ Urine

Output, Cool/Clammy skin, ↓ LOC, Dilated pupils, ↑ Blood sugar

Decompensated Extreme tachycardia, ↓ BP with narrow pulse pressure, Acute renal failure,

Continued decreasing LOC, Shift to anaerobic metabolism, Decreased ATP production, Production of lactic acid, & Metabolic & respiratory acidosis with hypoxemia

IrreversibleMultiorgan Dysfunction Syndrome Microvascular and organ damage are now irreversible

Death

Review of Types of Shock

Shock Type CVP PAWP SVR C.O. HR Comments

Hypovolemic ↓ ↓ ↑ ↓ ↑

Cardiogenic ↑ ↑ ↑ ↓ ↑

Neurogenic ↓ ↓ ↓ ↓ ↓

Septic ↓ ↓ ↓ ↑ ↑

Anaphylactic ↓ ↓ ↓ ↓ ↑

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Applying Hemodynamics

83

What is your interpretation of volume status?


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Vales after one 500cc fluid bolus of normal saline.

What is your interpretation of fluid status?

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What is your interpretation of volume status?


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Online Resources

https://education.edwards.com/series/icu#

www.pie.med.utoronto.ca

Documents

Objectives - img1.wsimg.com