1. Pulmonary Assmt & Physiology Flashcards
Ventilation is the
movement of air in (from the atmosphere) and out (from the body) to maintain appropriate concentrations of O2 and CO2.
Ventilation: Central Control
brain stem: primary control
-senses blood pH, decrease in PH –>ventilation is
stimulated.
-a decrease in pH = acidosis, which results in an
increase in the rate and/or depth of breathing
Ventilation: Peripheral Control
PaO2 “sensors” in the aortic arch: secondary control
-Senses PaO2 of blood, decrease in PaO2 –>ventilation
stimulated.
-Decrease in PaO2 = hypoxemia, which results in an
increase in the rate and/or depth of breathing
-Chronic PaCO2 retainers rely on mild hypoxemia for
ventilator drive. If the PaO2 is corrected to normal,
this may result in a decreased drive to breathe
(ventilate).
Ventilation:
What is the clinical indicator of ventilation? How do you know that your pt is ventilating normally?
You need to know the PaCO2 (NOT the PaO2).
Ventilation:
What is minute ventilation?
-Tidal Volume (Vt) x RR (resp rate) – easily seen on the ventilator of a pt who requires mechanical ventilation.
-Normal ventilation is ~4L/minute.
-An increase in minute ventilation = an increase in work of breathing.
Ventilation:
What is the primary muscle of ventilation?
-Diaphragm
-Anything that affects the “health” of the diaphragm (deconditioning, hypoxemia, acidosis, hypophosphatemia) will adversely affect ventilation.
Ventilation:
What is the position for optimal ventilation
-Upright sitting position
-Supine position is NOT good for ventilation; if a pt is in respiratory distress, the worse position for th pt is flat on his or her back!
Dead Space Ventilation:
Volume of air that does not participate in gas exchange
-Anatomic dead space: ~2 mL/kg of Vt
-We all have this; it’s normal
-No gas exchange at level of nose down to alveoli
-Alveolar dead space: pathologic, non-perfused alveoli,
PE
-Physiological dead space = anatomic dead space +
alveolar dead space
What results in increased dead space?
Pulmonary embolism!!
A clot in the pulmonary circulation (a pulmonary embolus): no blood flow past alveoli in that area of the pulmonary circulation. Figure 4 -1
Pulmonary perfusion: the main function of the pulmonary system is
Gas exchange. For gas exchange to occur normally, there needs to be ventilation. However, movement of air alone is not enough for normal gas exchange. There needs to be perfusion, movement of blood past alveoli.
Pulmonary perfusion is the movement of
blood through pulmonary capillaries.
-Any decrease in blood flow past alveoli (e.g. pulmonary embolus, low cardiac output states) will affect the ventilation/perfusion ratio and gas exchange.
Normal ventilation/perfusion ratio:
4L ventilation/min (V) / 5L perfusion/min (Q) = V/Q ratio
Ideal lung unit = 0.8 ratio, normal V/Q ratio
Any problem that alters ventilation (V) or perfusion (Q)
can result in abnormal gas exchange if compensatory mechanisms are not successful.
For example, even though it is not a pulmonary problem, a low cardiac output can result in poor gas exchange.
Won’t calculate V/Q ratios on text but will need to know that pulmonary problems will result in abnormal V/Q ratios (mild to extreme) depending upon the extent of the problem
Effect of Gravity on Pulmonary Perfusion
-In the upright position, most pulmonary blood is in the lower lung lobes (figure 4-2 A).
-When lying supine, most pulmonary blood is posterior (figure 4-2 B).
-Rarely are ALL lung units are perfused, but an example would be vigorous exercise (figure 4-2 C).
What are the clinical implications of Gravity on Pulmonary Perfusion
***You want the “good” lung down!!
-Large right lung pneumonia: if the pt is turned to the right (“bad” lung), more blood goes to the right, and the pt may become hypoxemia.
-Thus, the pt should not be turned to the right side.
***Perfusion of under-perfused anterior chest alveoli explains the improved oxygenation seen during PRONE positioning for severe hypoxemia.
**Normal V/Q Ratio
When there are no problems with either ventilation or perfusion, the pt will have normal gas exchange on room air (figure 4-3)
Abnormal V/Q ratio
-When there is a problem with ventilation or perfusion, there is a V/Q mismatch.
-The pt will develop hypoxemia on room air. However, providing oxygen will generally correct the hypoxemia until the etiology can be determined and addressed (figure 4-4)
Treatment of V/Q mismatch
Give O2.
Identify and treat underlying problem
Shunt
An extreme V/Q mismatch; even providing 100% FiO2 will NOT correct the hypoxemia (figure 4-5)
What is a shunt?
-Movement of blood from the right side of the heart to the left side of the heart without getting oxygenated; venous blood moves to the arterial side.
Normal physiological shunt:
Thebesian veins of the heart empty into the left atrium. This is why the normal oxygen saturation on room air is 95-99%; it cannot be 100% on room air due to this shunt.
(With supplemental oxygen, 100% saturation can be achieved)
Anatomic shunt:
two examples are:
- a ventricular septal defect
-atrial septal defect
Pathologic shunt:
ARDS!!
Blood goes through the lungs but does NOT get oxygenated resulting in REFRACTORY HYPOXEMIA.
Treatment of a pathologic shunt:
Administer OXYGEN and
PEEP!!! (Positive end-expiratory pressure)
- prevents expiratory pressure from returning to zero;
by keeping expiratory pressure POSITIVE, it…
-decreases surface tension of the alveoli, preventing
atelectasis.
-increase alveolar recruitment
-increase driving pressure, extends time of gas
transfer, allows for a decrease in FiO2 (fig. 4 - 6)
-With the addition of PEEp to the airway (provided in cm water pressure, i.e. 10 cm, 15 cm, etc.), hypoxemia will be addressed and the FiO2 may be decreased from 100%
Assessment of Oxygenation in the Critically Ill
Adequate oxygenation is the delivery of O2 to meet tissue demands at the cellular level. In order to achieve this, each of the following needs to occur:
-Adequate ventilation
-Transfer of O2 across alveolar-capillary membrane
-Presence of hemoglobin to carry O2
-Adequate CO (cardiac output) to deliver O2 to the
tissue bed
-Release of O2 from the hemoglobin molecule
-ability of cells to utilize O2
Oxygenation in critically ill: At the cellular level,
sufficient oxygen is needed for the production of adenosine triphosphate (ATP), which is needed for cell energy and life. Figure 4-7 shows how oxygen is needed for aerobic metabolism, along with the production of sufficient ATP for cell life. Without sufficient oxygen at the cellular level, lactic acid is produced (LACTIC ACIDOSIS), which is the evidence of anaerobic metabolism, organ failure, and eventual cell death.
Oxygenation in critically ill:
It is NOT sufficient to examine only ___ & ____
PaO2 & SaO2!!!
For example, a pt with sepsis/septic shock may have a normal PaO2, SaO2, and hemoglobin; clear lungs; and adequate ventilation and oxygen delivery, yet a lactate level of 10.
-This is lactic acidosis!
Why? Oxygen utilization is affected by sepsis/septic
shock and results in anaerobic metabolism at the
cellular level.
Clinical indicators of oxygenation in the critically ill
Table 4-1
Arterial Oxygen (PaO2), Saturation of arterial oxygen (SaO2), mixed venous oxygen saturation (SvO2), Oxygen content (CaO2), Oxygen delivery (DO2), Oxygen consumption utilization (VO2), alveolar-arterial (A-a) gradient.
Arterial Oxygen (PaO2): Normal; how it’s calculated/measured; Clinical Relevance
Normal: 80 -100 mmHg on room air
How it’s Calculated/Measured: Directly measured
Clinical Relevance: Less than 80 mmHg = hypoxemia (classified as mild, moderate, or severe)
Saturation of arterial oxygen (SaO2): Normal; how it’s calculated/measured; Clinical Relevance
Normal: 95 - 99% on room air
How it’s Calculated/Measured: Directly measured
Clinical Relevance: Direct relationship with PaO2; amount of hemoglobin combined with O2
Mixed venous oxygen saturation (SvO2): Normal; how it’s calculated/measured; Clinical Relevance
Normal: 60 - 75%
How it’s Calculated/measured: Direct measurement (pulmonary artery)
Clinical Relevance: Most sensitive indicator of oxygenation at the cellular level
Oxygen content (CaO2): Normal; how it’s calculated/measured; Clinical Relevance
Normal: 15 - 20 mL/100 mL blood
How it’s Calculated/Measured:
CaO2 = (Hgb x 1.39 x SaO2) + (PaO2 x 0.003)
Clinical Relevance: Severe anemia may result in hypoxia
Oxygen Delivery (DO2): Normal; how it’s calculated/measured; Clinical Relevance
Normal: 900 - 1100 mL/min
How it’s Calculated/Measured:
CaO2 x CO x 10
Clinical Relevance: Pump problems (heart) will decrease DO2
Oxygen consumption utilization (VO2): Normal; how it’s calculated/measured; Clinical Relevance
Normal: 250 - 350 mL/min
How it’s Calculated/Measured:
(SaO2 - SvO2) x Hgb x 13.9 x CO
Clinical Relevance: Low with septic shock
Alveolar -arterial (A - a) gradient: Normal; how it’s calculated/measured; Clinical Relevance
Normal: < 10 mmHg
how it’s calculated/measured:
PAO2 minus PaO2
(%FiO2 x 715) - PaCO2 (0.8 - PaO2)
Clinical Relevance: Calculates the difference between the alveolar oxygen and the arterial oxygen.
Indicates whether the gas transfer is normal and, if not, how bad the V/Q mismatch or shunt is; remember what normal is for the exam.
***For the exam:
Do not memorize the formulas.
-Remember that the assessment of oxygenation is more than just examining the PaO2 or SaO2.
-Consider the effects of severe anemia, low cardiac output, and an inability to utilize oxygen even when delivery is adequate (e.g. sepsis)
Most critical ill pts have continuous monitoring of oxygen saturation
oxygen saturation (SaO2) that is noninvasive ly measured with the use of a bedside pulse oximetry (SpO2). Although the normal SaO2 on room air is 95 - 99%, the goal for most critically ill pts is to maintain the SpO2 at 90% or greater, usually with supplemental oxygen. Note from the curve depicted in figure 4-8 that when the SaO2 is less than 90%, the PaO2 is less than 60 mmHg. When the PaO2 is less than 60 mmHg, cells begin to have difficulty maintaining aerobic metabolism (without compensation, i.e., an increase in heart rate or oxygen delivery).
***For the exam, you will need to understand the OXYHEMOGLOBIN-DISSOCIATION CURVE
Certain clinical conditions make hemoglobin “hold on” to oxygen molecules (the curve shifts to the LEFT). Other conditions allow hemoglobin to “release” the oxygen more easily to the tissue (the curve shifts to the RIGHT). See table 4-2 for conditions that shift the curve to the left and right; and figure 4 - 9 for an illusion of the oxyhemoglobin - dissociation curve.
Clinical conditions that cause a shift of the oxyhemoglobin-dissociation curve to the LEFT
-Alkalosis (low H+)
-Low PaCO2
-Hypothermia
-Low 2,3-DPG
Bad for tissues; SaO2 is high but O2 is stuck to Hgb
Clinical conditions that cause a shift of the oxyhemoglobin-dissociation curve to the Right
-Acidosis (high H+)
-high PaCO2
-Fever
-High 2,3 - DPG
Good for tissues; SaO2 is low but O2 is easily released to the tissues
Conditions that cause a shift to the left result in a __
a higher SaO2, but the tissues do not get needed O2 as readily
Conditions that cause a shift to the right result in a ___
somewhat lower SaO2, but the tissues receive O2 more readily
What is 2,3 - DPG?
2,3 - Diphosphoglycerate (2,3 - DPG)
It is an organic phosphate, found in RBCs, that has the ability to alter the affinity of Hbg for oxygen.
Decreased 2,3 -DPG results in
hemoglobin holding on to O2. (Table 4-3)
Increased 2,3 - DPG results in
hemoglobin more readily releasing O2 (table 4-3)
Effect of decreased 2,3 - DPG on Hgb Affinity for O2:
-Multiple blood transfusions of banked blood
-hypophosphatemia
-hypothyroidism
Result: Less O2 available to tissue
Effect of increased 2,3 - DPG on Hgb Affinity for O2:
-Chronic hypoxemia (e.g. prolonged time spent at high altitudes or chronic HF)
-Anemia
-Hyperthyroidism
Result: More O2 is available to tissues
