Functional residual capacity (volue of air in lungs at end of expiration)
Positive End Expiratory Pressure (presure in lungs at end of expiration)
Peak Expiratory Flow Rate (maximum airflow during forced expiration)
Ventilation/perfuson ratio (relationship of ventilation to perfusion in the lungs)
Minute ventilation (product of tidal volume times respiratory rate)
Tidal volume (volume of inspired air with each breath)
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.
Results from clinical states that interfere with adequate O2 transfer resulting in decrease in arterial tension (PaO2) and saturation (SaO2)
Results from insufficient CO2 removal manefesting by increase in arterial CO2 tension (PaCO2)
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.
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.
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
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.
At the lung apex
Electrophysiologic Properties of the Heart
Ability of specialized nerve cells to generate an impulse spontaneously & repetitively w/o neurohormonal control
Sensitivity to stimulation
The ability of the muscle fibers to contract in response to the electrical stimulation
The ability of cardiac myocytes to propagate electrical impulses across cell membranes in an orderly manner
Sychronous contraction of cardiac myocytes in response to efficient impulse delivery by the conduction system
Compensatory mechanism that makes cardiac myocytes unresponsive to stimulation
Impulse spreads across atria
Slight delay allows atria to fill - atrial kick
Not viable with life
Represents atrial depolarization
Precedes to QRS complex
Amplitude = 2-3 mm
Duration = 0.06 - 0.12 seconds
Generally rounded and upright
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