Transcript RT 30 Final Exam Review - Respiratory Therapy Files

RT 30 Final Exam Review
What is the blood flow through the
heart?
1) Blood enters the heart thru the inferior and superior vena cava
2) It then flows into the right atrium.
3) Thru the tricuspid valve into the Right Ventricle.
4) It then passes thru the pulmonic semilunar valve.
5) Then thru the pulmonary bed of the R. and L. lungs and back into the left atrium.
6) It then flows thru the bicuspid valve.
7) And into the left ventricle
8) Thru the aortic semilunar valve and into the aorta and systemic vascular system.
What is the normal conduction through
the heart?
SA
AV
BH
PF
What is endocarditis? What can cause it?
An inflammation of the inner layer of the heart, It usually involves the heart valves
Other structures that may be involved include the interventricular septum, the chordae
tendineae. Endocarditis is characterized by a prototypic lesion, the vegetation, which is a mass
of platelets, fibrin, microcolonies of microorganisms, and scant inflammatory cells
Injection of bacteria through dirty needles
What is Pericarditis?
•Fluid accumulation surrounding the heart, may lead to a life threatening condition called cardiac
tamponade
•Cardiac tamponade is compression of the heart that occurs when blood or fluid builds up in the
space between the myocardium and the pericardium
What is Myocarditis?
Myocarditis is most often due to infection by common viruses, less commonly nonviral
pathogens such as Borrelia burgdorferi (Lyme disease) or Trypanosoma cruzi, or as a
hypersensitivity response to drugs.
The definition of myocarditis varies, but the central feature is an infection of the heart, with an
inflammatory infiltrate, and damage to the heart muscle, without the blockage of coronary
arteries that define a heart attack (myocardial infarction)
What is Valvular disease?
Valvular heart disease is characterized by damage to or a defect in one of the four heart valves:
the mitral, aortic, tricuspid or pulmonary.
The mitral and aortic valves are the ones most frequently affected by valvular heart disease.
Valvular heart disease is characterized by damage to or a defect in one of the four heart valves:
the mitral, aortic, tricuspid or pulmonary.
The mitral and aortic valves are the ones most frequently affected by valvular heart disease.
Describe the following
CHFCADMICor PulmonaleHTN-
Pulm HTNWhat are characteristics and treatments of each?
What are the names of the coronary
arteries?
Left Coronary artery
Anterior Descending Artery
◦ Supplies anterior sulcus and apex
◦ Widow maker heart attack
Circumflex Artery
◦ Supplies posterior side of left ventricle
What are the names of the coronary
arteries?
Together supply most of left ventricle, left atrium, 2/3 of intra ventricular septum, half of intra
atrial septum, and part of right atrium
Right Coronary Artery
Posterior Descending Artery
◦ Supplies posterior intraventricular sulcus
Has numerous smaller branches
 Supplies anterior and posterior portions of
right ventricular myocardium, right atrium,
sinus node, posterior 1/3 of intraventricular
septum, and portion of base of right ventricle
Coronary Veins
Closely parallel the arterial system
oSome coronary venous blood enters the heart through the Thebesian
veins
◦ Thebesian veins empty directly into all chambers thus creating some
venous admixture lowering Pa02
What is a MI? What causes it, how is it
treated?
MONA
•Immediate assessment (<10 minutes)
•Measure vital signs (automatic/standard
BP cuff)
•Measure oxygen saturation
•Obtain IV access
•Obtain 12-lead ECG (physician reviews)
•Perform brief, targeted history and
physical exam;
focus on eligibility for fibrinolytic therapy
•Obtain initial serum cardiac marker levels
•Evaluate initial electrolyte and coagulation
studies
•Request, review portable chest x-ray (<30
minutes)
•Immediate general treatment
•Oxygen at 4 L/min
•Aspirin 160 to 325 mg
•Nitroglycerin SL or spray
•Morphine IV (if pain not relieved with
SVR and PVR formula
The Vascular System-Systemic Vascular Resistance (SVR)
Sum of all frictional forces opposing blood flow through the vascular circulation
SVR = Mean Aortic Pressure-Right Atrial Pressure x80
Cardiac Output
◦ Mean Aortic Pressure - Use Systolic Pressure (normal mean = 90mmhg)
◦ Right Atrial Pressure - Use Central Venous Pressure (normal mean = 4mmhg)
◦ Cardiac Output normal mean = 5L/min
PVR Formula:
MPAP – PCWP / CO x 80
The Vascular System-Blood Pressure
Systolic Pressure
Diastolic Pressure
◦ Pressure during contraction phase of heart
◦ Pressure during relaxation phase of heart
◦ Normal value: 90 – 140 mmHg
◦ Normal value: 60 – 90 mmHg
http://www.nlm.nih.gov/medlineplus/ency/anatomyvideos/000013.htm
Mean Arterial Pressure
MAP = (2 x diastolic pressure) + (systolic pressure)
3
A MAP of about 60 is necessary to perfuse coronary arteries, brain,
kidneys.
Cardiac Output
Cardiac Index
◦ Volume of blood pumped by the heart per minute divided by body
surface area
CI = CO
BSA
◦ Normal range of cardiac index is 2.5 - 4.0 L/min per square meter.
Low values can indicate cardiogenic shock
Stroke Volume
End-Diastolic Volume (EDV)
 Volume to which the ventricles fill during diastole
Formula: SV = EDV – ESV
Normal value: 60 – 130 ml/beat
Stroke Volume
Ejection Fraction (EF)
◦ Proportion of EDV ejected on each stroke
EF = SV
EDV
◦ Normal Value – 70%
Factors Affecting Stroke Volume
Preload
◦ Initial stretch of the ventricle
◦ The greater the preload, the greater the tension on contraction
Factors Affecting Stroke Volume
Afterload
◦ Force against which the heart must pump
◦ In clinical practice, left ventricular afterload equals systemic vascular
resistance.
Factors Affecting Stroke Volume
Contractility
◦ Amount of systolic force exerted by heart muscle at any given preload.
◦ Increases in contractility leads to higher EF, lower end systolic volume, and higher stroke
volume
Inotropic (drugs that increase cardiac contraction)
Chronotropic (drugs that increase cardiac rate)
Factors Affecting Stroke Volume
Contractility
◦ Decreases in contractility lead to
lower ejection fraction, higher end
systolic volume, and decreased
stroke volume.
Inotropism: Is any factor which affects
the contractility of the heart
◦ Positive Inotropism
◦ Higher stroke volumes for a given
preload: indicating an increase in
contractility.
Factors Affecting Stroke Volume
Contractility
 Negative inotropism
 Decreased stroke volumes for a given preload:
indicates a decrease in contractility
Factors Affecting Stroke Volume
Heart Rate (60-100)
Autonomic Nervous System
oSympathetic: fight or flight: HR, RR, BP, pupilary dilation
and bronchodilation.
oParasympathetic: rest and digest
Factors Affecting Stroke Volume
Heart Rate
◦ Cardiac output directly proportional to heart rate
◦ Relationship exists up to 160 to 180 beats/min
◦ Filling time for ventricles insufficient at higher rates
Arrhythmia Review
Initial Approach—Analysis
4 Questions
Rate?
◦ Normal
◦ Bradycardia, Tachycardia
Rhythm?
◦ Regular or Irregular
Are there P waves?
◦ Is each P wave related to a QRS with 1:1 impulse conduction?
QRS normal or wide?
Premature Atrial Contraction (PAC)
• Rate
• Rhythm
• P waves
• P → QRS
• Therapy

QRS
Normal
Sinus rate
Irregular—interrupted by PAC
Incomplete compensatory pause
Different morphology
Usually conducted with normal QRS
Treat underlying cause
34
Atrial Fibrillation

• Rate
• Rhythm
• P waves
• F → QRS
• Therapy
Atrial rate cannot be measured
Ventricular rate—variable
Irregular (irregularly irregular)
Absent (fibrillation waves)
Conduction irregular
Slow ventricular rate
Treat underlying cause
35
Atrial Flutter
QRS
Normal
• Rate
• Rhythm
• P waves
• F → QRS
• Therapy
Atrial rate 250-400/min (often 300)
Ventricular rate—variable
Regular (2:1 AV block common)
Absent (flutter waves)
Conduction regular (unless variable block)
Slow ventricular rate: terminate arrhythmia
Treat underlying cause
36
Self-Assessment
What are the rate and rhythm?
A
B
37
Clinical Correlation
This patient is unresponsive and
BP is 70/50 mm Hg.
What is the rhythm?
What is your next action?
38
PVC Morphology—Match the Name

•
Unifocal
PVCs
•
Multifocal
PVCs

•
•
Bigeminy

•
Torsades
Ventricular
Tachycardia

39
Ventricular Fibrillation (VF)
Ventricular Fibrillation (VF)
Polymorphic VT
TX without pulse:
◦ CPR
◦ DEFIB
◦ EPI/Mg 2g
Ventricular Tachycardia
Monomorphic*

*Sustained—requires intervention for >30 seconds
• Rate
• Rhythm
• P waves
• P → QRS
• Therapy
Atrial rate normal
Onset tachycardia abrupt
Regular
Present—obscured
Blocked—fusion complexes possible
Antiarrhythmic agent, cardioversion,
high-energy (defibrillation dose) shock
Polymorphic VT*
*Torsades de pointes—QT prolonged
• Rate
• Rhythm
• P waves
• P → QRS
• Therapy
Atrial rate normal (obscured)
Onset tachycardia abrupt
Irregular
Present—obscured
Blocked—fusion complexes possible
Unsynchronized high-energy shock,
magnesium (beneficial with baseline QTC
prolongation)
Ventricular Fibrillation
Coarse VF

• Rate
• Rhythm
• P waves
• P → QRS
• Therapy
Chaotic, uncountable
Onset abrupt
Irregular
Absent; no normal QRS complexes
Not applicable
Immediate shock(s)
Ventricular Fibrillation
Fine VF

• Rate
• Rhythm
• P waves
• P → QRS
• Therapy
Chaotic, uncountable
Onset abrupt
Irregular
Absent; no normal QRS complexes
Not applicable
Immediate shock(s)
Asystole
Agonal Complexes
Pulseless Electrical
Activity
•
•
•
•
•
Rate
Rhythm
P waves
P → QRS
Therapy
ASYSTOLE
Absent
None—“flatline”
Absent
Not applicable
CPR, vasopressor
Pulseless Electrical Activity (PEA)
ARTERIAL PRESSURE
• Rate
• Rhythm
• Therapy
Variable—depends on baseline rhythm
PEA is not a single rhythm but any
organized rhythm without a pulse
Identify and treat underlying cause
CPR, vasopressor
Self-Assessment
What are the rate and rhythm?
A
C
B
A
B
What rhythms do we defibrillate?
Cardiovert?
1.
2.
Epinephrine
• Epinephrine is a naturally occurring catecholamine with both - and
- adrenergic agonist activity
• Administer 1 mg (10 mL 1:10 000 IV bolus) every 3 to 5 minutes
during cardiac arrest
• Stimulation of -adrenergic receptors increases peripheral
vasoconstriction and as a result increases coronary and cerebral
blood flow
Epinephrine
Stimulation of -adrenergic receptors
• Increases heart rate, contractility, and conduction velocity
• Increases conduction through the atrioventricular node
• Decreases the ventricular muscle refractory period: these latter
effects may increase the likelihood of arrhythmias
Epinephrine
in Cardiac Arrest
Epinephrine may be administered
IV/IO
Endotracheal administration provides
uncertain doses
Remember to flush with 20 mL of
fluid and elevate the arm or leg
Special Considerations
Cautions—Contraindications
Important to REMEMBER:
High doses can cause arrhythmias
High doses do not improve survival
and may contribute to
postresuscitation myocardial
dysfunction
• A naturally occurring hormone, also known as antidiuretic
hormone (ADH)
• Causes vasoconstriction by directly stimulating smooth muscle
receptors
• Causes no increase in myocardial oxygen consumption during
CPR— no -receptor activity
Vasopressin
Clinical studies have shown vasopressin
equivalent to epinephrine for treatment of cardiac arrest
Vasopressin
Vasopressin can be
substituted for the first or
second dose of epinephrine
Give 40 units IV/IO bolus
Coronary perfusion pressure
Vital organ blood flow
Median frequency VF
Cerebral oxygen delivery
Bradycardia
First-Degree AV Block
Sinus Node
P
• Underlying sinus rhythm
• One P wave
• PR interval >0.20
second
• One P wave for each
QRS
AV Node
AV Nodal
Tissue
>0.20 seconds
QRS <0.12
His-Purkinje System
57
Second-Degree AV Block—Mobitz I
Wenckebach Phenomenon
Sinus Node
• Underlying sinus rhythm
• P wave fails to
periodically
conduct
• PR interval prolonged
• One P wave for each
QRS until block
P
AV Nodal
Tissue
>0.20 seconds
PR interval
X
QRS
His-Purkinje System
58
Second-Degree AV Block—Mobitz II
PR intervals unchanged


Sinus Node
P
Block
• Underlying sinus rhythm
• One P wave
• PR interval usually
normal, no prolongation
• One P wave for each QRS
until sudden block and
dropped QRS

AV Node
Often AV
Normal
Nodal
Tissue
Often
normal
QRS
complex
His-Purkinje System
59
Third-Degree AV Block—Junctional Escape
P waves unrelated to QRS
Sinus Node
• Underlying sinus rhythm
(usual)
• Escape junctional rate 40-60
• PR interval variable
• P waves unrelated to QRS
P

QRS from
AV-His
escape
AV Node
QRS <0.12
• Narrow QRS = block above
His junction
His Purkinje System
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AV Block—Which Type?




Properties of Heart Muscle
Excitability
◦ Ability to respond to electrical, chemical, or mechanical stimulation
Properties of Heart Muscle
Excitability
This is important as the heart will respond to defibrillation, cardioversion, and
medication
Properties of Heart Muscle
Automaticity
◦ Ability of cardiac muscle to initiate a spontaneous electrical impulse (only cell capable
of doing this)
◦ Highly developed in specialized areas – pacemaker or nodal tissue
Automaticity
Automaticity of the heart is produced by spontaneous and repetitive depolarization of certain
cardiac cells, known as pacemaker cells.
The depolarization of these cells leads to the generation of action potentials, which are
electrical signals that are propagated throughout the cardiac muscle tissue and result in
contractions. Understanding depolarization is essential to comprehending cardiac
electrophysiology as a whole.
Automaticity
Depolarization:
The process of depolarization occurs at the cellular level and involves changes in the electrical
environment of a cell. This electrical environment is determined by the difference in the
concentrations of charged particles between the inside and outside of the cell.
Automaticity
Resting Membrane Potential:
At rest, the inside of a myocardial cell has a charge that is more negative than its surroundings.
Therefore, the cell is said to have a negative resting membrane potential. This potential is
normally around -90 millivolts, meaning the charge inside the cell is 90 millivolts lower than the
surrounding environment.
Properties of Heart Muscle
Conductivity
◦ Ability to radiate electrical impulses
◦ Impaired in response to necrotic tissue from ischemic
injury (MI)
Contractility
◦ Ability to contract in response to an electrical impulse
◦ Impaired by hypertrophy, cardiomyapathy, CHF
Activation of
Central Chemoreceptors
by changes in arterial Pco2
Medulla
Chemoreceptors
IN
H2O
CO2
H2CO3
H+
HCO3-
CO2
CSF
BBB
plasma
capillary
Performing an EKG
Basic Electrocardiography-Terms
Polarization
◦ Difference in electrical potential between two points in
tissue; the resting state of cardiac muscle
Basic Electrocardiography
Peripheral and central chemoreceptors respond to changes in blood chemistry, mainly CO2,
pH and O2.
Low O2 = increase HR and RR
 High CO2 (H+ in medulla) = Increased HR and RR
Low pH (aciditc) = Increase HR and RR
Baroreceptors:
Increase pressure = Increased HR, decreased pressure = increased HR
And contractility
Basic Electrocardiography-Terms
Depolarization
◦ Influx of sodium into the interior portion of the cells
causing muscle contraction
Repolarization
◦ Rapid return of the cell to the polarized state
EKG Paper
The Electrocardiogram
P Wave
◦ Produced by atrial depolarization
◦ Normally 0.06 to 0.11 seconds in duration
The Electrocardiogram
QRS Complex
◦ Produced by ventricular depolarization
◦ Normally 0.03 to 0.12 seconds in duration
◦ Repolarization of the atria occurs
simultaneously with QRS and is hidden by the
QRS complex
The Electrocardiogram
T Wave
◦ Produced by ventricular repolarization
◦ Normally 0.14 to 0.26 seconds
The Electrocardiogram
PR Interval
◦ Time from beginning of atrial depolarization to beginning of
ventricular depolarization
◦ Normal interval is 0.12 to 0.20 seconds
The Electrocardiogram
RR Interval
◦ Time from peak of one QRS complex to the next QRS
complex
◦ Normally 0.6 to 1.0 seconds
◦ Used to measure total cardiac cycle
The Electrocardiogram
PP Interval
◦ Time from beginning of one P wave to the beginning of the next P
wave
◦ Normally equal to RR interval
◦ Also used to measure total cardiac cycle
The Electrocardiogram
Event
Time
P Wave
0.06 – 0.11 Seconds
PR Interval
0.12 – 0.20 Seconds
QRS Complex
0.03 – 0.12 Seconds
T Wave
0.14 – 0.26 Seconds
PP/RR Intervals
0.6 – 1.0 Seconds
ECG Leads
Lead I:
◦ (-) Negative Electrode on Right Arm
◦ (+) Positive Electrode on Left Arm
Sinus Bradycardia
Rate less than 60
Rhythm is regular
P wave prior to each QRS/QRS for each P wave
PR interval normal
QRS interval normal
Sinus Tachycardia
Rate greater than 100
Rhythm is regular
P wave prior to each QRS/QRS for each P wave
PR interval normal
QRS interval normal
Sinus Tachycardia
Causes
•
•
•
•
•
•

•
•
•
•
•
Fever
Anxiety
Pain
Dehydration
Anemia
Hypoxemia (generally first sign)
If symptomatic:
Anxiety
Feelings of fear or panic
Feelings of a pounding chest
Treat underlying cause
http://www.youtube.com/watch?v=cKXrzLrQOCc
Atrial Fibrillation
Rate 100-160 BPM
Rhythm is irregular
P waves absent and replaced by irregular electrical activity
QRS interval normal to narrow
Most common arrhythmia
Atrial Fibrillation
Causes:
◦
◦
◦
◦
Disorganized electrical impulses that originate in the atria and pulmonary veins
Hypertension
Hyperthyroidism
Primary heart disease
If symptomatic:






Palpitations
SOB
Exercise intolerance
Clot formation within heart/lungs/brain/legs Ect.
Dizziness/ somnolence/ decreased LOC
http://www.youtube.com/watch?v=70QE1poMZ1E&feature=related
Atrial Fibrillation
Treatment
• Anti-Coagulants
• Beta Blockers
 If symptomatic:
• Immediate Cardioversion
• Oxygen
http://www.youtube.com/watch?v=1rcg6Ce7p18
ECG Leads
Lead II
◦ Negative Electrode on Right Arm, Positive Electrode on Left Leg
◦ Used Most Commonly in Acutely Ill Patients With Leads Placed on Chest
Rather Than on Limbs
ECG Leads
Lead III
◦ Negative Electrode on Left Arm, Positive Electrode on Left Leg
Leads I, II, and III Comprise Einthoven’s Triangle And Present Electrical
Activity of The Heart From Three Different Orientations
Electrocardiogram
Einthoven’s triangle
• Three standard limb leads
• Voltage differences
between corners of triangle
• We will use “Lead II”
◦ Right shoulder to left leg
03 Sept. 2013
92
EKG-Lab.ppt
Limb Leads
ECG Leads
Precordial Leads
◦ Leads V1, V2, V3, V4, V5, And V6
◦ V1 – Positive Electrode Placed at Right Sternal Margin And
Fourth Intercostals space
ECG Leads
Precordial Leads
◦ Successive Leads Placed Laterally to The Left With V6 at Mid
Axillary Line
◦ Electrical Activity Measured From Six Different Locations And
Depicted Differently For Each Lead
Precordial Leads
Sinus Bradycardia
Rate less than 60
Rhythm is regular
P wave prior to each QRS/QRS for each P wave
PR interval normal
QRS interval normal
Sinus Tachycardia
Rate greater than 100
Rhythm is regular
P wave prior to each QRS/QRS for each P wave
PR interval normal
QRS interval normal
Sinus Tachycardia
Causes
If symptomatic:
•
•
•
•
•
•
•
•
•
•
Fever
Anxiety
Pain
Dehydration
Anemia
Hypoxemia (generally first sign)
Anxiety
Feelings of fear or panic
Feelings of a pounding chest
Treat underlying cause
http://www.youtube.com/watch?v=cKXrzLrQOCc
Atrial Fibrillation
Rate 100-160 BPM
Rhythm is irregular
P waves absent and replaced by irregular electrical activity
QRS interval normal to narrow
Most common arrhythmia
Atrial Fibrillation
Causes:
◦
◦
◦
◦
Disorganized electrical impulses that originate in the atria and pulmonary veins
Hypertension
Hyperthyroidism
Primary heart disease
 If symptomatic:





Palpitations
SOB
Exercise intolerance
Clot formation within heart/lungs/brain/legs Ect.
Dizziness/ somnolence/ decreased LOC
http://www.youtube.com/watch?v=70QE1poMZ1E&feature=related
Atrial Fibrillation
Treatment
• Anti-Coagulants
• Beta Blockers
 If symptomatic:
• Immediate Cardioversion
• Oxygen
http://www.youtube.com/watch?v=1rcg6Ce7p18
Supraventricular Tachycardia
Rate 140-220
Rhythm is regular
P waves absent (buried in the T wave)
QRS interval usually normal
PR interval - impulses stimulating the heart are not being generated by the sinus node, but instead
are coming from a collection of tissue around and involving the atrioventricular (AV) node
Supraventricular Tachycardia
•Causes:
CAD
Thyroid disease
COPD
Caffeine
Stress
• If symptomatic:





Palpitations
Dizziness
Anxiety
Chest pain
Loss of consciousness
http://www.youtube.com/watch?v=ReJo4aclOw8
Supraventricular Tachycardia
Treatment
 Vagal manuvers
 Carotid massage
 Cardioversion: Electrical/Chemical (Adenosine)
 Medications
 Oxygen
 Ablation
 Pacemaker
http://www.youtube.com/watch?v=xLzRFAT9uFA
Basic ECG Interpretation
NSRo Is the rate regular?
o Is the rate between 60-100?
o Is their a P wave prior to each QRS/ QRS for each P wave?
o Is the PR interval normal - .12 to .2 Sec? (less than 1 big box)
o Is the QRS interval less than .12 Sec? (less than 3 little boxes)
PHARMACOLOGY
(indications/dose and classification)
Adenosine
Atropine
Amiodarone
Lidocaine
Epinephrine
Dopamine
Levophed
Vasopressin
Depolarizing Agents
Bind to acetylcholine receptor sites causing a postsynaptic membrane depolarization
Prevention of repolarization causes the postsynaptic ending to become refractory and
unexcitable, resulting in muscle flaccidity
Non-Depolarizing Agents
Produce paralysis and muscle weakness by competing
with acetylcholine for binding at the receptor site
Prevention of the binding of acetylcholine prevents
depolarization of the site, thereby preventing muscle
contraction
Action

Action
Prevents acetylcholine from binding at the receptor
site
Shorter acting than non-depolarizing agents
Will cause total muscle paralysis in 60 to 90
seconds that lasts from 10 to 15 minutes
Do not have reversing agents
Generic name Proprietary name
Succinylcholine
Anectine
Indications
- Short acting paralytic ideal for intubation or
similar procedures


Competitive inhibition of acetylcholine at
muscle
post-synaptic receptor site
Effects felt in 2 to 10 minutes and last for 30 to 60
minutes
May be reversed by cholinesterase inhibitors, e.g.,
Neostigmine
Generic Name
Proprietary Name
Tubocurarine
d-tubocurarine
Pancuronium
Pavulon
Metocurine
Metubine
Vecuronium
Norcuron
Rocuronium Zemuron,
Esmeron
Indications
- Need for longer term paralysis
- Patient-ventilator synchrony
- Muscle relaxation during surgery
- Indications
- Reduction of intracranial pressure
- Immobility in trauma patients- Minimize oxygen consumption
Indications for NMBAs
Endotracheal intubation
Muscle relaxation during surgery
Enhancement of patient-ventilator synchrony
Reduction of intracranial pressure in intubated patients
Minimizes oxygen consumption
Facilitation of procedures or diagnostic studies
Maintenance of immobility, e.g., trauma patients (Flail Chest)
Narcotis and Analgesics
Know opiods (high, mod, low potency)
Morphine
Oxymorphone
Fentanyl
Methadone
Hydromorphone (Dilaudid)
Demerol
Percocet
Oxycontin
Codeine
Narcotic Antagonist
Narcan
Sedative and Hypnotics
Ativan
Versed
Xananax
Valium
Deprivan
Haldol
Pentothal
Pentobarbital
Phenobarbital
Reversal of Benzos
Ramazicon
Other Meds
Diruretics: Diamox, Lassix, Mannitol, Carbonic anyhydrase inhibitors
Steroids: Side effects, indications…
HEMODYNAMICS
Values PAP, CVP, PCWP
Causes of each to increase/decrease
Indications for PICC, A-lines, Central and
PA lines
Troubleshooting PA and A-line tracings
Cardiac output assessments
Formulas
CVO2=
DO2=
C(a-v)=
SVO2=
EF=
PFT’S
Spirogram
Lung Volumes & Capacities
Lung Volumes & Capacities
Examples of Flow-Volume Loops in Disease
States
Examples of Flow-Volume Loops in Disease
States
SVC
Purpose:
To determine the maximum amount of the volume that can be
taken in and exhaled with a single breath
FVC
To measure flow rates and lung volumes in order
to determine the presence of obstructed or
restricted lung impairment
Spirometry
Forced vital capacity (FVC)
◦ Technique – subject breaths normally for several breaths, then inspires maximally
and exhales as forcefully and fully as possible
◦ Should be within 200 mL of VC
Spirometry
Forced expiratory volume (most commonly FEV1)
◦ Volume which can be exhaled in one second using maximum patient effort
◦ Determined from the FVC
◦ Decrease in value indicates obstructive changes in small airways
Spirometry
Spirometry
FEF25%-75%
◦ Average expiratory flow rate of the middle 50% of the FVC
◦ Measured in liters per second
◦ Indicates flow from medium and small airways
◦ Changes from smoking occur in medium airways prior to changes in small airways
MVV
To measure muscle strength during times of increased
exertion
Measurements of RV/TLC
Nitrogen Washout
Helium Dilution
Body Box
Spirometry
Maximum voluntary ventilation (MVV)
◦ Calculates the maximum volume of gas that a patient can ventilate in one minute
◦ Technique – subject is directed to breathe rapidly and deeply for 12 to 15 seconds;
the total volume inspired or expired is measured; the volume is extrapolated to one
minute
DLCO
To evaluate the ability of the lungs to take in oxygen
from the air, and transfer the oxygen across the lungs
into the blood stream
Interpreting the PFT Report
The FEV1/FVC ratio is a good place to start; reduced (<70%) with
obstructive lung disease
If TLC less than 80% of predicted normal and FEV1/FVC is normal,
restrictive disease is present.
If DLCO is <80% of normal, a diffusion defect is present.
◦ Reduced surface area = emphysema
◦ Thickened AC membrane = pulmonary fibrosis
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