Objectives - img1.wsimg.com
Transcript of 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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AIRWAY TROUBLESHOOTING
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
AIRWAY TROUBLESHOOTING
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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ELEMENTS OF ABGS: NORMAL VALUES
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.
ELEMENTS OF ABGS: NORMAL VALUES
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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ELEMENTS OF ABGS: NORMAL VALUES
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.
ELEMENTS OF ABGS: NORMAL VALUES
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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ELEMENTS OF ABGS: NORMAL VALUES
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?
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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
15
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)
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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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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
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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 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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ARDS Treatment/Management
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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
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Non-Invasive Oxygenation Strategies• High Flow Nasal Cannula• Proning• Inhaled vasodilators
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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
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HFNC
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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
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HFNC
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HFNC Protective Measures• Surgical mask over patient’s nose/mouth
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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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Proning Mechanics
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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)
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Proning• System-based approach
– Nurses– Respiratory Therapists– Technicians– Physician
• Equipment– Pillow (2 or 3)– Sheet
AACN Procedure 19
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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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Proning Risks• Increased need for sedation/paralysis• Increased hemodynamic instability• Transient desaturation• Accidental extubation• Accidental dislodgement of lines, tubes
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Proning Contraindications• Spinal instability• Unstable fractures especially face / pelvis• Open wounds • Shock• Pregnancy• Tracheal surgery
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Proning Steps
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Proning
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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).
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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/
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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)
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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)
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 15, 1958)
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.
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.
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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
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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
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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:
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Transcutaneous Pacing
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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.)
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Temporary Generator
(Transvenous or Epicardial)
Single Chamber or Dual Chambers
www.Medtronicacademy.com
Pacer cables
Disposable Non-disposable
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Epicardial Wires
Anatomy of the temporary pacemaker circuit, Alex Yartsev
Epicardial Wires
WWW.MEDTRONICACADEMY.COM
Transvenous
PacingTransvenous wires
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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.
www.medtronicacademy.com
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Universal Pacemaker Code
• 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
Universal Pacemaker Code
• 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
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Universal Pacemaker Code
• Other examples include:
– V O O
– A A I
• Letters 4 and 5 of code indicate such functions as:
– Multiprogrammability
– Rate responsiveness
– Communication possibilities
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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.
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Pacemaker Identification
• Example of a Pacemaker Rhythm
• Note the “spike” preceding each complex
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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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A Pacemaker Rhythm
• Pacemaker stimulus seen as a vertical spike
• Spike will precede the response of the heart
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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
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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.
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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
Pacemaker Malfunction
• 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.
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Pacemaker Malfunction
• 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.
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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
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Pacemaker Rhythms
• Ventricular Pacing: Rate: ? with inappropriate sensing
– Note pacemaker spikes in the QRS complexes)
• Treatment: Report Immediately to MD
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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
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Complications
• Temporary
– Pain
– Tissue damage if defibrillated
– Failure to correctly ID pacer malfunction
– Infection, bleeding
– Pneumothorax
– Perforation of ventricle
– Instability of the system
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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)
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Implantation
• Temporary
– At bedside: transvenous, transcutaneous
– Cardiac Cath Lab (CCL): transvenous
– In surgery: epicardial
• Permanent
– CCL
– Surgery
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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
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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
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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
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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
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Pacemaker Rhythms
Atrial Pacing
Ventricular Pacing
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Pacemaker Rhythms
• Atrial Pacing
– Rate: 58 with Complete Capture
– Treatment: none; continue to monitor
– Note: can’t evaluate sensing-no intrinsic beats seen
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Pacemaker Rhythms
• Interpretation: Ventricular Pacemaker
– Rate: 79 with Complete Capture and appropriate sensing
– Treatment: None; continue to monitor
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Pacemaker Rhythms• A-V Sequential Pacing (both atrial and ventricular spikes seen)
– Rate: A = 56, V = 56
– Complete Capture
– Treatment: none; continue to monitor
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Pacemaker Rhythms
• Interpretation:
– A - V Sequential Pacing Rate: 63 with complete capture
• Treatment: none; continue to monitor
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Pacer Malfunction
• Failure to Capture
– Lead displacement or fracture
– Sensing problems
– Battery depletion
WWW.MEDTRONICACADEMY.COM
www.medtronicacademy.com
www.medtronicacademy.com
www.medtronicacademy.com
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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
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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
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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
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How’s the patient doing?
Blood Pressure
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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.
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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
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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.
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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
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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
Normal: 100-250 dynes
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 Artery:Systolic 20-28 mmHgDiastolic 8-12 mmHgMean 8-15 mmHg
Pulmonary Vascular Resistance (PVR)
Most sensitive measure of afterload for the right ventricle
Normal: 100-250 dynes
Pulmonary Artery Systolic Pressure > 35 mmHg indicates pulmonary hypertension.
Pulmonary Artery Catheter - Pulmonary Artery Pressures – PAMP
Pulmonary Artery:Systolic 20-30 mmHgDiastolic 8-12 mmHgMean 8-15 mmHg
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:Systolic 20-30 mmHgDiastolic 8-12 mmHgMean 10-15 mmHg
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.
The other half of the Pie – SvO2 & ScVO2Normal: SvO2 - 60%-80% & ScvO2 - 70%
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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The other half of the Pie – SvO2 & ScVO2Normal: SvO2 - 60%-80% & ScvO2 - 70%
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?
Applying Hemodynamics
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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?
Applying Hemodynamics
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Online Resources
https://education.edwards.com/series/icu#
www.pie.med.utoronto.ca