Unit 4 - Wk 6 Physiology

Front 1

Tachypnea

Back 1

Rapid breathing

Front 2

Apnea

Back 2

Absence of breathing

Front 3

Hyperpnea

Back 3

Breathing deeper and more rapid than normal

Front 4

Hypercapnea

Back 4

High levels of carbon dioxide in the blood

Front 5

Hypoventilation

Back 5

Decreased amount of air being moved in and out of lungs

Front 6

Hyperventilation

Back 6

Increased amount of air being moved in and out of lungs

Front 7

Minute Volume

Back 7

The amount of air moved in and out of lungs per minute

Front 8

Respiratory Minute Volume

Back 8

total volume moved in and out of lungs per minute

Front 9

Alveolar Minute Volume

Back 9

Amount of air available for gas exchange per minute

Minute ventilation = (tidal volume)(breaths/min)

Front 10

Dead Space

Back 10

Regions of the respiratory system that contain air but are not exchanging °2 and CO2 with blood are considered dead space (conductive bronciholes)

Front 11

Alveolar Ventilation

Back 11

Alveolar Ventilation = (Tidal volume - dead space)(breaths/min)

Front 12

Cardiac output =

Back 12

heart rate x stroke volume

Front 13

Resting Tidal Volume

Back 13

500 ml

Front 14

Average Volume of the anatomic Dead Space

Back 14

150 ml

Front 15

normal respiration rate

Back 15

14-16 breaths per minute (15)

Front 16

Alveolar Minute Volume

Back 16

Breaths per minute x (volume per breath - anatomic dead space) = 15 x (500-150) = 5250 ml/minute

Front 17

Steps in the Mechanics of Respiratoin

Back 17

1. Ribs expand and diaphragm contracts (pleural volume increases, intra pleural pressure decreases)

2. Patm > Palv, alveolar volume increases as lungs expand thus decreasing the pressure in the alveoli below atmospheric pressure
3. As air enters lungs, increased volume of air raises pressure and when pressure in the alveoli = atmospheric presure than air flow ceases (Patm =Palv)

4. Reverse (ribs/diaphragm relax, decreases alveolar and pleural volume increasing pressure and forcing air out due to Patm < Palv)

Front 18

Back 18

Mechanics of breathing

On inspiration, alveolar and pleural pressure decreases bc of increased surface area (Pressure = Force/Area); on expiration alveolar and pleural pressure increases due to decreased volume of the cavity which forces air out

Front 19

Back 19

Residual Volume: Amount of air left in lungs after full exhalation

Tidal Volume: Air moved in and out during normal resting respiration

Vital Capacity: Total amount of air the lungs can move in and out per breath

Front 20

How would left heart failure influence ventilation?

Back 20

Left heart failure would result in pulmonary edema which would lead to fluid accumulation in the lungs. This would initially reduce ventilation that would lead to compensatory changes resulting in increased rate and depth of breathing

Front 21

How would right heart failure influence ventilation?

Back 21

Right heart failure would result in decreased blood flow to the lungs. This would initially reduce oxygen delivery and carbon dioxide removal which would lead to compensatory changes resulting in increased rate and depth of breathing

Front 22

How would pulmonary edema affect ventilation?

Back 22

Fluid would decrease the volume of the alveoli

Fluid would decrease gas exchange

Fluid would alter the compliance of the lungs

Fluid would affect ventilation/perfusion ratio

Front 23

How would muscle pathologies influence ventilation?

Back 23

Decreased muscle function would lead to the inability to change volumes of the chest cavity as the ribs or diaphragm would either be more difficult to move or not move at all; (paralysis, guillain barree syndrome, myasthenia gravis, neurological disorders or poisons)

Front 24

How will obstructive lung blockage affect volume and capacities?

Back 24

Increase residual volume

Front 25

How will restrictive lung disease affect lung volumes and capacities?

Back 25

Decrease total lung capacity

Front 26

FEV1

Back 26

Volume of air that can be expired in the first second of forced maximal expiration; it's normally 80% of the forced vital capacity

FEV1/FVC = .8

Front 27

Tidal Volume

Back 27

Volume inspired or expired with each normal breath

Front 28

Inspiratory Reserve Volume

Back 28

Volume that can be inspired over and above the tidal volume; is used during exercise

Front 29

Expiratory Reserve Volume

Back 29

Volume that can be expired after the expiration of tidal volume

Front 30

Residual Volume

Back 30

Volume that remains in the lungs after a maximal expiration; cannot be measured by spirometry

Front 31

A person with a tidal volume (Vt) of 0.5L is breathing at a rate of 15 breaths/min. The PC02 of his arterial blood is 40 mmHg, and the PC02 of his expired air is 36 mmHg. What is his rate of alveolar ventilation?

Back 31

Front 32

Inspiratory Capacity

Back 32

Sum of tidal volume and IRV

Front 33

Functional Residual Capacity

Back 33

Sum of ERV and residual volume
Volume remaining in the lungs after a tidal volume is expired
Includes the residual volume so it CANNOT BE MEASURED BY SPIROMETRY

Front 34

Vital Capacity/Forced Vital Capacity

Back 34

Sum of the tidal volume, IRV, and ERV; volume of air that can be forcibly expired after a maximal inspiration

Front 35

Total Lung Capacity

Back 35

Sum of all four lung volumes; volume in the lungs after a maximal inspiration; includes residual volume, so it cannot be measured by spirometry

Front 36

How would asthma affect FEV1?

Back 36

In obstructive lung diseaes, FEV1 is reduced more than FVC so that FEV1/FVC is decreased

Front 37

How is FEV1 affected in fibrosis?

Back 37

In restrictive lung disease, both FEV1 and FVC are reduced and FEV1/FVC is either normal or is increased

Front 38

Dorsal Respiratory Group

Back 38

Inspiration; generates the basic rhythm for breathing

Input: Vagus and glossopharyngeal
Output: Phrenic nerve to diaphragm

Front 39

Ventral Respiratory Group

Back 39

Expiration; not active during passive breathing; activated during exercise when expiration becomes an active process

Front 40

Apneustic Center

Back 40

Stimulates inspiration, producing deep/prolonged inspiratory gasps (apneusis)

Front 41

Pneumotaxic Center

Back 41

Upper pons

Inhibits inspiration; regulates inspiratory volume and respiratory rate

Front 42

Hering-Bruer Inflation Reflex

Back 42

Prevents overinflation of lungs; stretch receptors in smooth muscle of bronchi/bronchioles send inhibitory signal through vagus to DRF/apneustic center

Front 43

Where are dentral chemoreceptors located?

Back 43

Medulla; must occur IN THE CSF

CO2 crosses BBB, reacts with water to decrease pH

Front 44

Neural Effects of H+ and C02

Back 44

Increased PC02 = increased ventilation

Front 45

Where are peripheral chemoreceptors located?

Back 45

Cartid bodies located at bifurcation of common carotids
Aortic bodies located above and below the aortic notch

Front 46

relatoinship between arterial P02 and breathing rate

Back 46

Decreases in arterial P02 stimulate peripheral chemoreceptors and increase breathing rate; when P02 decreases below 60 mmHg breathing rate rapidly increases

Front 47

Increases in arterial PC02

Back 47

Stimulate peripheral chemoreceptors and increase breathing rate; potentiate stimulation of breathing caused by hypoxemia

Front 48

How is venous PC02 affected by exercise?

Back 48

Increases during exercise bc excess C02 produced by exercising muscle is carried to the lungs in venous blood

Front 49

How is dead space affected by exercise?

Back 49

pulmonary blood flow increases because cardiac output increase during exercise. As a result, more pulmonary cpaillaries are perfused and more gas exchange occurs.
The distribution of V/Q ratios throughout the lung is more even during exercise then when at rest, thus there is a decrease in physiologic dead space.

Front 50

Cheyne-Stokes Breathing Explained

Back 50

When a person overbreathes, thus blowing off too much carbon dioxide from the pulmonary blood while at the same time increasing blood oxygen, it takes several seconds before the changed pulmonary blood can be transported to the brain and inhibit the excess ventilation. By this time, the person has already overventilated for an extra few seconds. Therefore, when the overventilated blood finally reaches the brain respiratory center, the center becomes depressed an excessive amount. Then the opposite cycle begins.

Front 51

Sleep Apnea

Back 51

Loud snoring/labored breathing after falling asleep; snoring interrupted by long silent period during which no breathing occurs; periods of apnea result in significant decreases in P02 and increases in PC02, which stimulate respiration -> sudden attempts to breathe (loud snorts, gasps, followed by snoring and repeated episodes of apnea)

Front 52

Daltons Law of Partial Pressures

Back 52

Partial pressure = (total pressure)(fractional gas concentration)

Front 53

Pressure of air around us

Back 53

760 mmHg

Front 54

Assume that total pressure is atmospheric and the fractional conc. of 02 is 0.21. What is the partial pressure of dry inspired air (P02)?

Back 54

P02 = 760 mmHg x 0.21 = 160 mmHg

Front 55

Why must the total pressure be modified for tracheal air?

Back 55

Tracheal air is humidified (H20 vapors) at 37C and thus the calculation is modified to correct for the partial pressure of H20, which is 47 mmHg

P tot = (760 mmHg - 47 mmHg = 713 mmHg

P02 (tracheal) = (713)(.21) = 150 mmhg

Front 56

Physiologic shunt

Back 56

2% of the systemic cardiac output bypasses the pulmonary circulation; the resulting admixture of venous blood w oxygenated arterial blood make sthe P02 of arterial blood slightly lower than that of alveolar air

Front 57

Why is the partial pressure of P02 decreased to 100 and the PC02 increased to 40 in alveolar air?

Back 57

P02: 02 has diffused from alveolar air into pulmonary capillary blood, decreasing the P02 of alveolar air

PC02: C02 has been added from pulmonary capillary blood into alveolar air

Front 58

What does putting oxygen on a pt who is saturating at 100% do?

Back 58

Increase dissolved oxygen (which is normally about .3 ml 02/100ml blood

Front 59

What things shift the Hb-02 curve to the right

Back 59

Right shifts occur when the affinity of Hg for 02 is decreased; facilitates unloading of 02 from arterial blood to tissues

Front 60

What things shift the Hb-02 curve to the left

Back 60

Left shifts occur when the affinity of Hg for 02 is increased (high Hg sat at lower P02)

Front 61

What is the difference in P02 between alveolar air and systemic arterial blood (pulmonary capillaries)?

Back 61

No difference; they are equilibrated at 100

Front 62

What is the difference between PC02 in alveolar air vs systemic arterial blood (pulmonary capillaries)?

Back 62

No difference; they are equilibrated at 40

Front 63

What is the main form of C02 transport in the blood?

Back 63

HC03 (from hydration of C02 in the rBCs); 90%

Front 64

Carbonic Anhydrase

Back 64

Hydrates C02 in RBCs to form HC03 + H

Front 65

Chloride Shift

Back 65

HC03 leaves RBCs in exchange for Cl- and is transported to the lungs in the plasma (HC03- is major form in which C02 is transported to the lungs)

Front 66

What buffers H+ inside RBCs?

Back 66

Deoxyhemoglobin

Front 67

What happens to C02 once it is in the lungs?

Back 67

All the tissue reactions occur in reverse

HC03- enters RBCs in exchange for Cl-. HC03 recombines with H+ -> H2C03 which decomposes into C02 and H20; thus C02 generates in the tisuses is expired

Front 68

Why is there a slight left shift in CO poisoning?

Back 68

Binding of CO to Hg increases the affinity of remaining sites for 02, causing a shift of the curve to the left

Front 69

How does a physiologic shunt affect V/Q?

Back 69

V/Q < normal
Low ventilation

Front 70

How does a physoilogic dead space affect V/Q?

Back 70

V/Q > normal
Wasted ventilation

Front 71

Where in the lung is V/Q/ highest?

Back 71

At the apex (top of the lung); P02 is highest and PC02 is lower bc there is more gas exchange (bc blood flow is slowest here)

Front 72

Where in the lung is V/Q lowest?

Back 72

At the base (base of the lung)
P02 is lowest and PC02 is higher bc there is less gas exchange

Front 73

Acidemia

Back 73

Condition that results in a lower than normal pH (7.1-7.3), <7.1 = fatal

Front 74

Alkalemia

Back 74

Higher than normal pH, 7.44-7.69, >7.70 can be fatal

Front 75

Acidosis

Back 75

A condition that adds acid to the blood or removes bases from the blood

Front 76

Alkalosis

Back 76

A condition that adds bases to the blood or removes acids from the blood

Front 77

Respiratory Acidosis

Back 77

Respiratory acidosis is a condition that occurs when the lungs cannot remove all of the carbon dioxide the body produces. This disrupts the body's acid-base balance causing body fluids, especially the blood, to become too acidic; can be caused by an increased rate of respiration (short trip to higher elevation, hyperventilation, respiratory stimulants)

Kidneys will increase bicarbonate secretion to balance

Front 78

Respiratory Alkalosis

Back 78

Respiratory alkalosis is a condition marked by low levels of carbon dioxide in the blood due to breathing excessively.

can be caused by anxiety, fever, hyperventilation

Front 79

A 6 year old child is seen in the emergency room. He is wheezing and has a bluish hue to the mucosal membranes. His mother indicates the child has been diagnosed with asthma. Does the child have respiratory acidosis or alkalosis?

Back 79

Acidosis (not blowing off their C02?

Front 80

A 55 year old man is seen in the internal medicine clinic. His major compliant is shortness of breath, a condition that has become progressively worse over the last 5 years. He is a 2 pack a day smoker. Stat labs reveal the following:


Plasma concentrations
HCO3- = 40 meq/l
K+ = 4.5 meq//l
HCT = 45+
Hb = 12 mg/dl
Plasma protein 6.0/dl
Glucose = 80 mg/dl
BUN = 12 mg/dl
Creatinine = 1.4 mg/dl
Arterial PCO2 = 70 mmHg
pH (arterial) = 7.35

Does he have respiratory acidosis or alkalosis?

Back 80

Acidosis (not blowing off his C02)

Front 81

A 23 year old woman is in the delivery room. She is in hard labor. Her Lamaze coach has instructed her to “puff and blow” when the labor pains become intense. She was told to bring a small paper bag with her to breathe into during the labor pains. The purpose of the bag is to prevent her form developing respiratory acidosis or alkalosis?

Back 81

Respiratory alkalosis; she hyperventilates, is not blowing off C02 and thus becomes mroe acidic, preventing respiratory alkalosis

Front 82

What side chain on hemoglobin and albumin allows them to function as protein buffers?

Back 82

Histidine; these residues can donate and accept H+ at physiologic pH making them good buffering agents

A buffer functions effectively within one pH unit of its pKa