Shields Lecture 5 Flashcards
0
Q
Discuss bronchial bloodflow.
A
- very small portion (1 to 2%) of the LV output
* provides tracheobronchial tree with arterial blood
1
Q
Identify the tracheobronchial tree blood supply down to the terminal bronchioles.
A
Bronchial arteries arising from the aorta or intercostal arteries
2
Q
Discuss pulmonary bloodflow
A
- Entire RV output
- supplies lungs with mixed venous blood
- undergoes gas exchange with air in the pulmonary capillaries
3
Q
Identify the blood supply to the terminal bronchioles
A
Respiratory bronchioles, alveolar ducts, alveolar sacs and alveoli receive oxygen directly by diffusion from the alveolar air
4
Q
Describe the role of the lungs as a reservoir for blood volume
A
- 450 mL of total blood volume
- 20 to 30% increase in blood volume in heart failure patients
- increased intrathoracic pressure decreases blood volume
- changes from supine to upright posture decrease blood volume by 27%
5
Q
Compare the pulmonary vascular resistance to systemic vascular resistance
A
pulmonary vessels:
- much less resistance to bloodflow
- are more distensible and compressible due to lower intravascular pressures
- PVR is 1/10 of SVR
6
Q
Compare the effect afterload on the right ventricle compared to left ventricle
A
The right ventricle does not pump against high pressures normally so it fails during acute pulmonary hypertension due to being very sensitive to changes in Afterload. The left ventricle has a greater workload, higher metabolic demand and normally pumps against extremely high pressures to perfuse the head. If the left ventricle fails, it bulges into the septum, pushing the septum into the right ventricle and compressing the stroke volume of the right ventricle.
7
Q
Describe the effect of airway pressure on zero order capillaries
A
If alveoli collapse, pulmonary capillaries collapse and there is little blood flow through them= less shunt
8
Q
Discuss the role of alveolar collapse in pulmonary vascular resistance
A
As closing capacity exceeds FRC = less PVR
9
Q
Identify the number of first order pulmonary capillaries and their blood volume
A
300 million
150 mL
10
Q
Define recruitment and distention as they relate to perfusion
A
Increased blood flow increases mean pulmonary artery pressure, which opposes hydrostatic forces and exceeds critical opening pressure in previously unopened vessels, opening
New parallel Pathways (recruitment) and lowering pulmonary vascular resistance. As perfusion pressure increases, transmural pressure gradient of pulmonary blood vessels increases, causing vessel distention of already opened vessels (widening of vessels). This increases radii and decreases resistance to bloodflow. Distention occurs after recruitment occurs
11
Q
Compare and contrast alveolar effects and extra alveolar effects on capillary size
A
As lung volume increases, extra alveolar vessels get wider ( diameter increases ) and resistance decreases within those vessels. Intra-alveolar vessels get smaller and tighter as they are elongated. Diameter decreases and resistance increases in those vessels as alveoli expand
12
Q
Describe the effect of increased blood flow On pulmonary vascular resistance
A
As arterial blood pressure, venous pressure, and pulmonary artery pressure increases, pulmonary vascular resistance decreases. vessels are distensible and resistance depends on how many vessels are opened, not on the caliber of the vessel
13
Q
Describe the effect of increasing lung volume on pulmonary vascular resistance
A
Pulmonary vascular resistance is increased when lung volume is low. As you begin to inhale, as you get to FRC, you have much less resistance
14
Q
List five factors that increase PVR
A
- Hypoxia
- Low pH of mixed venous blood
- nor epinephrine & epinephrine
- Alveolar hypercapnia
- histamine
- angiotensin
- thromboxane and endothelin
- alpha-adrenergic agonists
- stimulation of sympathetic nervous system
- catecholamines
- serotonin
- atelectasis
- acidosis
15
Q
List five factors that decrease PVR
A
Bradykinin Nitric oxide Beta-adrenergic agonist Acetylcholine Stimulation of parasympathetic innervation Isoproterenol Milrinone Flo lan – epoprosterenol Theophylline Increase cardiac output and pulmonary blood volume
16
Q
Describe the effect of alpha-1 agonist, beta-2 agonist and V-1 agonists on PVR
A
Alpha one increases
Beta-2 and V-1 decrease
17
Q
Define hypoxic pulmonary vasoconstriction
A
Contraction of smooth muscle in the walls of small arterioles in a hypoxic region that occurs in response to low alveolar PO2 ( less than 70 mmHg ) directs blood flow away from hypoxic regions of the lung
18
Q
Identify the triggering action for HPV
A
Low alveolar PO2
19
Q
Describe the effect of HPV on PVR and bloodflow
A
HPV begins to occur at alveolar PO2 in the range of 100 to 150 mmHg and increases until PaO2 falls to about 20 to 30 mmHg. It diverts mixed venous blood flow away from poorly ventilated areas of the long by locally increasing vascular resistance. mixed venous blood is sent to better ventilated areas of the long
20
Q
List 4 drugs that decrease HPV
A
Beta agonist Calcium channel blockers Inhalation anesthetics Minoxidil Nitro vasodilators Theophylline
21
Q
Describe why lower regions of the lung receive more bloodflow
A
Intravascular pressures in more gravity dependent portions of the lines are greater than those in the upper regions. Because the pressures are greater in the more gravity dependent regions of the line, the resistance to bloodflow is lower in lower regions of the lung owing to more recruitment or distention of vessels in these regions
22
Q
Compare V/Q ratios in West’s Zone 1
A
Zone 1: pulmonary arterial pressure falls below alveolar pressure, ventilation is greater than perfusion, VQ ratio is high no flow occurs
23
Q
Compare V/Q ratios in West’s zone 2
A
Zone2: pulmonary arterial pressure increases related to hydrostatic pressure so better ventilation perfusion matching occurs, bloodflow only occurs when there is a gradient and is based on respiratory and cardiac cycles
24
Compare V/Q ratios in West zone three
Pulmonary arterial pressure increases and exceeds alveolar pressure. More perfusion than ventilation , VQ ratio is low , blood flow is continuous
25
Identify two factors that increase the prevalence of zone
Hemorrhage and positive pressure ventilation
26
Describe zone four and it's significance
Some fluid is forced out of the capillary and into the perivascular space . this zone is very small as alveolar vessels are closed by increased PVR from collapsed alveolus
27
List eight factors contributing to pulmonary edema
Increased capillary permeability: ARDS ,oxygen toxicity, inhaled circulating toxins
Increased capillary hydrostatic pressure: increased left atrial pressure from infarct or mitral stenosis, over administration of IV fluids
Decreased colloid osmotic pressure: protein starvation , dilution of blood proteins by hemodilution ,proteinuria
Decreased interstitial hydrostatic pressure: rapid evacuation of pneumothorax
Insufficient lymphatic drainage: tumors, interstitial fibrosing diseases
Other causes: high-altitude pulmonary edema, head injury, drug overdose
28
List for causes of negative pressure pulmonary edema
```
Post extubation laryngeal spasm
Epiglottitis
Croup
Choking/foreign body
Strangulation/hanging
Endotracheal tube obstruction
Tumor/goiter
Near drowning
Direct suctioning endotracheal tube adapter
```
29
List four causes of hypoxemia
Hypoventilation: drugs, inadequate minute ventilation
Diffusion issue: CHF, ARDS
Shunt: anatomic, atelectasis
Ventilation/perfusion mismatch: COPD
30
Describe the clinical result of VQ mismatch
Hypoventilation
Hypoxemia
Hypercarbia
31
Identify the most common cause of hypoxemia during anesthesia
Ventilation perfusion inequality
32
Describe the typical distribution of perfusion
Most of the blood flows to the bottom of the lung
33
Compare the distribution of blood flow and ventilation
Bloodflow and ventilation are both high at the base of the lung; most ventilation occurs in the lower lung because the alveoli are more compliant
34
Describe the effect of anesthesia on FRC, lung compliance, and airway resistance
F RC and lung compliance decrease
| Airway resistance increases
35
Identify the effect of moving from the top to the bottom of the lung on V/Q ratio , perfusion, Alveolar PO2, and Alveolar PCO2
* V/Q ratios high at the top and low at bottom
* perfusion increases dramatically from the top-of-the-lung to the bottom of the lung
* PO2 is higher at the top-of-the-lung while CO2 is higher at the bottom of the lung
36
Discuss anatomic and physiologic shunt as they relate to ventilation and bronchial/ thesbian circulations
Shunt refers to blood that enters the arterial system without entering ventilated areas of the lung. Bronchial and thespians circulations constitute anatomic shunt, while blood passing through the poorly ventilated lung represents physiologic shunt. Anatomic shunt is the systemic venous blood entering the left ventricle without having entered the pulmonary vasculature. Physiologic shunt corresponds to physiologic dead space
37
Define pulmonary capillary oxygen content as it relates to alveolar PO2
Oxygen content of the blood at the end of the ventilated and perfused pulmonary capillaries
38
Define arterial oxygen content as it relates to arterial PO2
Oxygen content of arterial blood in ml of O2/ml blood plus the oxygen in the unaltered mixed venous blood coming from the shunt
39
Define mixed venous oxygen content as it relates to mixed Venous PO2
Oxygen content of mixed venous blood
40
Describe the effect of shunt on increasing inspired oxygen concentrations & PaO2
Increasing inspired oxygen concentration increases PAO2 and subsequently PaO2. Varying degrees of shunt will limit the effect of PaO2 such that eventually increasing inspired 02 has no effect on PaO2
41
Discuss expected VQ ratios and healthy patients
In a healthy patient almost all ventilation and bloodflow (95%) go to compartments close to a VQ ratio of about 1.0. Bloodflow and ventilation are matched very evenly and almost no bloodflow occurs to unventilated regions
42
Describe the effects of lung disease on VQ ratios
In a patient with lung disease, V/Q distribution is not equally distributed. This blood will be poorly oxygenated & will depress PO2. Considerable ventilation will go to units without perfusion so CO2 will not be eliminated
43
Describe compensation for VQ abnormalities in patients with lung disease
Increase minute ventilation via central and peripheral chemoreceptors
HPV and pulmonary bronchoconstriction assist in matching perfusion & ventilation
Dissociation curve for CO2 is linear (favors elimination)
Dissociation curve for O2 is (flat favors loading of oxygen)
44
Identify factors that determine exchange-rates of gases across membranes
Thickness of the respiratory membrane
Surface area of the membrane
Pressure difference of the gas between the two sides of the membrane
Diffusion coefficient of the gas in the substance of the membrane
45
Define Ficks law
The net diffusion rate for the gas across the fluid membrane is proportional to the difference in partial pressure ,the area of the membrane, and inversely proportional to the thickness of the membrane. Combined with the diffusion rate from Grahams law, it is a means for calculating exchange-rates for gases across membranes
46
Identify two factors which determine the concentration of a gas in a solution using Henry's law
Partial pressure of the gas
| Solubility coefficient
47
Compare solubility coefficients for oxygen, carbon dioxide, carbon monoxide and nitrogen
Oxygen 0.024
Carbon dioxide 0.57
Carbon monoxide 0.018
Nitrogen 0.012
48
Identify the mechanism responsible for most carriage of oxygen in the plasma
Hemoglobin
49
Describe the effect of increasing FIO2 from 100 to 600 mm Hg oxygen-carrying capacity
Has little increase
50
Identify the average capillary exposure/ transit time
0.7 seconds
51
Identify the normal time period required for diffusion to occur
0.3 seconds
52
Describe the effect of lower alveolar PO2 on diffusion and arterial PO2
Decreases diffusion
53
Compare arterial and tissue PO2 and the effect on diffusion
Arterial PO2 : 95 mm Hg
| Tissue PO2 : 40 mm Hg
54
Discuss the mechanism of diffusion of carbon dioxide across the alveolar septa
Simple diffusion based on a concentration gradient
55
Discuss the mechanism of diffusion of oxygen across the alveolar septa
Via concentration gradient
56
Define Graham's Law
When gases are dissolved in liquids, the relative rate of diffusion of a given gas is proportional to its solubility in the liquid & inversely proportional to the square root of its molecular mass
57
Compare the diffusion capacity of oxygen relative to carbon dioxide , nitrous oxide, carbon monoxide, & nitrogen
```
Oxygen :1.0
CO2 :20.5
NO2: 14.0
CO: 0.80
N2 : 0.55
```
58
Calculate the amount of oxygen dissolved in the plasma given a PO2
0.003 X given value
59
Identify the maximum amount of oxygen which may combine with a gram of hemoglobin
1.34 mL / gram of hemoglobin
60
Identify the determinant of the equilibrium point of reaction that determines the amount of oxygen that binds to hemoglobin in the red blood cells
The amount of oxygen hemoglobin is exposed to or P02
61
List conditions that decrease diffusion capacity
Thickening of the barrier: interstitial or Alveolar Edema/fibrosis, sarcoidosis, and scleroderma
Decreased surface area: emphysema, tumors, low cardiac output, low pulmonary capillary blood volume
Decreased uptake by erythrocytes: anemia, low Pulmonary capillary blood volume
Ventilation perfusion mismatch
62
Describe the two major elements of diffusion capacity and their components
Membrane capacity is affected by factors involving movement between alveoli and blood. Reaction time with hemoglobin is affected by factors involving movement into capillaries and uptake by red blood cells.
Components of membrane capacity: the V/Q mismatch or Alveolar – arterial oxygen gradient, gas solubility, increased thickness of membrane, and pathology
Components of reaction time with hemoglobin: pulmonary blood volume & flow, cardiac output, hemoglobin concentration, affinity for hemoglobin, unfavorable red blood cell shape, transit time for red blood cell
63
Calculate oxygen content of the blood given hemoglobin concentration & oxygen saturation
(1.34 X hemoglobin X SPO2) + ( 0.003 X PO2)
64
Define p50 for hemoglobin saturation
The point on the oxyhemoglobin dissociation curve where 50% saturation occurs (which is around 26 to 27 mmHg partial pressure of oxygen on the curve)
65
List five determinants of SVO2
```
Hemoglobin concentration
Hemoglobin saturation
Cardiac output
Oxygen consumption
Oxygen utilization
```
66
List the six clinical conditions that may decrease SV02
```
Anemia
Hypovolemia
Fever/shivering
Seizures
Pain/exercise
Hyperthyroidism
```
67
Describe the structure of hemoglobin in relationship to it's oxygen-carrying capacity
Protein portion (globin) consists of four linked polypeptide chains attached to a protoporphyrin (heme) group. Each of the four polypeptide chains can bind with an oxygen molecule or CO
68
Calculate the oxygen-carrying capacity for varying hemoglobin concentrations and PO2
?g Hgb/ 100 ml X 1.34 ml O2/g Hgb
69
List five factors that may alter P50 and how the oxygen hemoglobin saturation curve is affected
Factors: temperature, pH, PCO2, DPG levels, type of hemoglobin.
High temp, DPG, PCO2, low pH= right shift
Low temp, DPG, PCO2, high pH= left shift
70
List four clinical conditions shifting the oxyhemoglobin dissociation curve to the left
Decrease in hydrogen ion concentration, PCO2, temperature, and DPG
Increase in pH
Fetal hemoglobin, carboxyhemoglobin, methemoglobin
71
Define the Bohr effect as it relates to shifts in the oxyhemoglobin dissociation curve and oxygen loading/unloading
Rightward shift combined with high PCO2 means more unloading at lower pH for acidotic tissues.
Rightward shift allows for greater oxygen unloading at higher PCO2, allowing for improved oxygen delivery and more room on hemoglobin for carrying of CO2
72
List four clinical conditions shifting the oxyhemoglobin dissociation curve to the right
Increase in hydrogen ion concentration, PCO2, temperature, DPG
Sickle cell
73
Describe the effect of carbon monoxide poisoning on oxygen-carrying capacity and the oxygen dissociation curve
Interferes with oxygen transport by combining with hemoglobin to form carboxyhemoglobin.
Hemoglobin concentration and PO2 are normal, but oxygen content is greatly reduced. Oxyhemoglobin curve shifts to the left
74
Discuss mechanisms for dealing with carbon monoxide poisoning
Increased FI O2 promotes elimination of carbon monoxide (decreases half-life from four hours to less than one hour)
75
Discuss the pathophysiology of met hemoglobinemia and clinical considerations
Oxygen can only bind if hemoglobin is in the Ferrous State. Removal of iron atom reduces to ferric state and is unable to bond with oxygen ( LA, nitros, nitrates, sulfonamides)
76
Describe P50 considerations of aberrant hemoglobins
If curve is shifted to the left, the P 50 decreases: myoglobin
Sickle cell anemia: P50 increases
77
List six anesthetic considerations for patients with sickle cell
```
Avoid hypoxia
avoid acidemia
Avoid hypovolemia
Avoid hypothermia
Transfuse to preoperative PCV 30%
No Tourniquets
```
78
Describe how carbon dioxide is transported in the arterial & venous blood
CO2 is transported in the blood in physical solution, chemically combined with amino acids and as bicarbonate ions
79
Calculate the amount of CO2 dissolved in the blood given a PC02
0.067 X given CO2 value
80
Compare the CO2 carrying capacity of reduced hemoglobin compared to oxyhemoglobin
Reduced hemoglobin is 3.5 times as effective as oxyhemoglobin.
Hemoglobin is more of a base when reduced, resulting in increased carrying capacity of carbon dioxide
81
Define the Haldane effect in relationship to the ability of hemoglobin to carry CO2
Fall in hemoglobin saturation increases buffering ( more H ion capacity) and increases carbon dioxide carriage
82
Define chloride shift as it relates to red blood cell electrical neutrality and carbonic acid
It preserves electrical neutrality
More bicarbonate ions leave red blood cells that hydrogen ions; hamburger shift occurs and allows excess bicarbonate ions to diffuse out of the cell in exchange for chloride ions
83
Compare the carboxyhemoglobin dissociation curve to the oxyhemoglobin dissociation curve
Within normal physiologic range of PCO2, the curve is nearly straight-line.
CO2 dissociation curve is shifted to the right for greater levels of oxyhemoglobin, and shifted to the left for greater levels of deoxyhemoglobin
84
Describe how a weak acid behaves in solution such as blood
Acts as an acid by donating a hydrogen
85
Compare the three mechanisms responsible for hydrogen regulation
```
Buffer systems( rapid but incomplete )
ventilator responses (less rapid)
Renal responses (slow, but produces almost nearly complete correction of pH)
```
86
Identify four buffering systems the body incorporates in regulating acid-base balance
Hemoglobin
Bicarbonate
Phosphate
Protein/intracellular buffers/buffers of interstitial fluid/ bone
87
Identify the most effective intracellular buffering system
Due to its high concentration of intracellular proteins, protein buffering systems are the most potent
88
Discuss rationale for why the bicarbonate system is the most important buffering system in the body
It's element can be regulated by both the kidneys and the lungs
89
Describe the role of ventilation in regulating hydrogen ion concentration
Doubling alveolar ventilation eliminates sufficient CO2 to increase pH to 7.6. Decreasing alveolar ventilation to one fourth of normal decreases pH to 7.0
90
Describe renal regulation of hydrogen ion concentration
In the presence of acidosis hydrogen ion is excreted
| bicarb is excreted in alkalosis
91
List five anesthetic consideration in acidosis
Decreased sympathetic tone
Increased arrhythmogenicity of volatile agent increased potassium with succinylcholine
Augmentation of neuromuscular blockade
Potentiation of depressant effects of sedatives and anesthetic agents on CNS & circulatory system (increased non-ionized fraction and increased penetration into brain)
92
Identify the role of the Medulla in regulating respiration
Regulate the initiation of inspiration: dorsal and forced expiration: ventral
93
Identify the role of the pons in regulating respiration
Apneustic Center prolongs respiration
| Pneumotaxic Center regulates respiratory rate
94
Discuss the role of the dorsal respiratory group in the regulation of respiration
Located on dorsal surface of the medulla, inspiratory area is the pacemaker , sends action potentials to the diaphragm and external intercostals and receives inhibitory signals from the Vagus and glossopharyngeal
95
Describe how the Apneustic & Pneumotaxic center regulate rate and depth of respiration
Apneustic : stimulatory, is located in the lower pons, promotes deep and prolonged inspiration (excitatory), works with Pneumotaxic Center to control rate & depth of respiration
Pneumotaxic: inhibitory, located in the upper pons, transmits inhibitory signals to the DRG to avoid overinflation, affects respiratory rate indirectly by inhibition of over inflation
96
Identify the location of the central chemo receptors and the primary regulatory element
Anterolateral surface of the medulla that is sensitive to chemical changes ( CO2)
97
Identify the two peripheral chemo receptors and the primary regulatory element
Carotid bodies and aortic bodies
| Respond to changes in Pa02 , PaCO2 , blood pressure and pH
98
Discuss the effects of PO2 on the carotid body chemoreceptor
Respond mainly to low PaO2 but not high PaO2
Activation does not occur until PaO2 is less than 50 mmHg
Not stimulated by oxygen saturation abnormalities such as carbon monoxide poisoning
99
Identify the location and innervation of the pulmonary stretch receptors and how they are stimulated
They are located in walls of bronchi and bronchioles , are activated when stretched tending to inhibit inspiration ( Hering-Breuer reflex when TV > 1.5 ml) and causes shortening of exhalation when the lung is deflated. Inhibitory signals are carried centrally by the vagus nerve and protects against over inflation
100
Identify the location and innervation of the irritant receptors and how they are stimulated
They live between airway epithelial cells
are stimulated by noxious gases (smoke, dust, cold air) and impulses travel up the Vegas.
They also have responses to release histamine, playing a role in bronchoconstriction in asthma
101
Identify the location and innervation of the J receptors and how they are stimulated
Juxtacapillary or J receptors are in Alveolar walls close to capillaries. Impulses pass up the vagus nerve and result in rapid shallow breathing.
They are activated by engorgement of pulmonary capillaries and increased interstitial fluid volume of the alveolar wall
102
Describe the effect of pH on respiration
Reduction in pH stimulates ventilation
103
Describe the integrative effect of PCO2, PO2 and pH on respiration
Low pH shifts the response curve to the left. Exercise enhances the response to hypoxia even if PaCO2 is not raised, possibly due to lactic acidosis, afferents from muscle, or catecholamine secretion
104
Describe the effects of different anesthetic agents on the PCO2 response curve
Shifts response curve to the left, less sensitive to CO2.
| Normal ~40, Mac ~45, Mac 1.5 ~ 48, opioids ~ 55
105
Describe the effects of different anesthetic agents on the PO2 response curve
Barbiturates produce dose-dependent depression of medullary and pontine ventilatory centers. Benzodiazepines produce dose-dependent decrease in response to PCO2. Ketamine does not produce significant depression of ventilation, with PCO2 unlikely to increase > 3 mmHg.
106
Describe the effects of inhaled anesthetics on the control of ventilation
All volatile anesthetics depress minute ventilation, which is compensated to a degree by increased respiratory rate. All inhalation agents depress the ventilatory response to PaCO2 & PaO2
107
Describe the effect of the cortex & limbic system on the control of ventilation
The cortex may exert voluntary control to increase or decrease tidal volume and or respiratory rate.
The limbic system and hypothalamus may exert control through various emotional states
