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FIO2
Fraction of inspired oxygen concentration
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FRC
Functional residual capacity (volue of air in lungs at end of expiration)
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PEEP
Positive End Expiratory Pressure (presure in lungs at end of expiration)
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PEFR
Peak Expiratory Flow Rate (maximum airflow during forced expiration)
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V/Q
Ventilation/perfuson ratio (relationship of ventilation to perfusion in the lungs)
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VE
Minute ventilation (product of tidal volume times respiratory rate)
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VT
Tidal volume (volume of inspired air with each breath)
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Acute Respiratory Failure
- Results when either the transfer of O2 or CO2 between the atmosphere and the blood is inadequate.
- Not a disease, it is a condition that occurs as a result of one or more diseases involving the lungs or other body systems.
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Hypoxemia
Results from clinical states that interfere with adequate O2 transfer resulting in decrease in arterial tension (PaO2) and saturation (SaO2)
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Hypercapnia
Results from insufficient CO2 removal manefesting by increase in arterial CO2 tension (PaCO2)
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Hypoxemic Respiratory Failure
- aka oxygenation failure because the primary problem is inadequate O2 transfer between the alveoli and the pulmoary capillary bed.
- Commonly defined as PaO2 of 60 mm Hg or less or when the patient is recieving an inspired O2 concentration of 60% or greater.
- Disorders that interfere with O2 transfer into the blood include pnuemonia, pulmonary edema, pulmonary emboli, and alveolar injury related to alveolar stress/ventilator induced lung injury. In addition low CO states can cause hypoxemic respiatory failure.
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Hypercapnic Respiratory Failure
- aka ventilatory failure because the primary problem is insufficient CO2 removal.
- Commonly defined as PaCO2 above normal (greater than 45 mm Hg) in combination with acidemia (arterial pH less than 7.35)
- Disorders that compromise lung ventilation ans subsequent CO2 removal include drug overdoses with CNS depressants, neuromuscular diseases and trauma or diseases involving the spinal cord. Acute asthma is also associated with hypercapnic respiratory failure.
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Mechanisms that cause Hypoxemic Respiratory Failure
- 1. mismatch between ventilation (V) and perfusion (Q), commonly referred to as V/Q mismatch. This is one of the most common causes
- 2. Shunt. This is one of the most common causes.
- 3. Diffusion limitation
- 4. hypoventilation
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Ventilation-Perfusion (V/Q)
- Normal lung the volume of blood perfusing in the blood per minute is 4-5 L and is approximately equal to the volume of fresh gas that reaches the alveoli each minute (4-5 L)
- In a perfectly matched system each portion of the lung would get 1 mL of air for each 1 mL of blood flow.
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Ventilation-Perfusion Mismatch
At the lung apex
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Electrophysiologic Properties of the Heart
- Automaticity
- Excitability
- Conductivity
- Contractility
- Refractoriness
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Automaticity
Ability of specialized nerve cells to generate an impulse spontaneously & repetitively w/o neurohormonal control
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Excitability
- Sensitivity to stimulation
- The ability of the muscle fibers to contract in response to the electrical stimulation
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Conductivity
The ability of cardiac myocytes to propagate electrical impulses across cell membranes in an orderly manner
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Contractility
Sychronous contraction of cardiac myocytes in response to efficient impulse delivery by the conduction system
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Refractoriness
- Compensatory mechanism that makes cardiac myocytes unresponsive to stimulation
- During systole:
- -Absolute
- -Relative
- -Supernormal period
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SA Node
- Impulse spreads across atria
- 60-100 BPM
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AV Node
- Slight delay allows atria to fill - atrial kick
- 40-60 BPM
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Purjinke Fibers
- 20-40 BPM
- Not viable with life
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Normal EKG
- Complexes:
- -P wave
- -QRS complex
- -ST segment
- -T wave
- Intervals:
- -PR Interval
- -QRS Interval
- -QT Interval
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P Wave
- Represents atrial depolarization
- Precedes to QRS complex
- Amplitude = 2-3 mm
- Duration = 0.06 - 0.12 seconds
- Generally rounded and upright
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PR Interval
- Measured from the beginning of the P wave to beginning of QRS complex
- Time required for impluse to spread through the atria, bundle branches & purjinke fibers to the point of ventricular activation
- Normal = 0.12 - 0.20 seconds
- - < means impulse may have originated elsewhere than SA node
- - > means conduction delay through atria or AV node
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QRS Complex
- Represents ventricular depolarization (contraction)
- Configuration depends on lead
- Normal = 0.04 - 0.12 seconds
- If prolonged can mean disturbance in conduction through bundle branches AKA bundle branch block
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ST segment
- Represents early ventricular repolarization
- Normally isoelectric
- -Elevation or depression >1 mm or 1 small box
- -Depression may indicate ischemia or digoxin toxicity
- -Elevation may indicate myocarduial injury
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T wave
- Represents ventricular repolarization
- Amplitude is 0.5mm
- - Usually positive deflection
- - May be tall, peaked, inverted or flat with ischmia, K or Ca imbalances & medications
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QT interval
- Time required for ventricular depolarization & repolarization
- Measured from the beginning of QRS complex to end of T wave
- Duration varies with age, sex, & HR
- - with regular rhythm - QT should not exceed 1/2 the distance between 2 consecutive R waves
- -Normal is 0.34 - 0.43
- -Hold QT meds if QT is greater than 0.44 seconds
- -Prolonged QT can lead to Torsades de Pointes (form of VT refractory to treatment)
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U wave
- Represents repolarization of the His-Purjinke fibers
- May not appear on EKG
- Follows the T wave
- Deflection is upright
- if prominent may indicate hypercalcemia, hypokalemia, or dig toxicity
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Sinus Breadycardia Causes
- Inferior wall MI
- Excessive vagal stimulation
- Valsalva meneuver
- Carotid sinus massage
- Hypoxia
- Hypothyroidism
- Hypothermia
- Increased IOP
- Obstructive Jaundice
- Increased ICP
- Medications
- - Beta blockers
- -CCB
- -Digitalis
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