cell bio test 4 block 4

pressure in left ventricle

120/0

average pressure in pulmonary artery?

15 mmHg

Safe range of the partial pressure of oxygen delivered to peripheral tissues is ?

20 - 40 mm Hg

Bicarb concentration in arterial blood?

22-28 mEq/L

Bicarb concentration in venous blood?

23-29 mEq/L

pO2 in venous blood?

30-40 mm Hg

pCO2 in arterial blood?

35-45 mmHg

pCO2 in venous blood?

41-51 mm Hg

1 hr stay at 18.000 ft (unacclimatized aviator breathing oxygen) will still cause ?% deterioration of his/her mental status !!!

50%

pH in venous blood?

7.31-7.41

pH in arterial blood?

7.35-7.45

Oxygen saturation in venous blood?

75%

pO2 in arterial blood?

80-100 mm Hg

When does the A-a gradient indicate abnormal gas exchange (some V/Q mismatch or impaired gas exchange)?

>25 mm Hg indicates abnormal gas exchange

Oxygen saturation in arterial blood?

>95%

An individual's inspired PO2 was 150 mm Hg and his alveolar PCO2 was 40 mm Hg. If this person's alveolar ventilation was then doubled, his alveolar PO2 would be expected to change by (assume a R value of 1.0) A. 20 mm Hg B. 25 mm Hg C. 40 mm Hg D. 50 mm Hg E. no change

A •20 mm Hg •If alveolar ventilation doubles, then PCO2 is halved so 40/2 = 20. so PAO2 would increase by 20.

Are the Extra-alveolar vessels affected by intrapleural pressure, interstitial pressure or alveolar pressure?

Affected by intrapleural and interstitial pressures changes; Not affected by alveolar pressure

If the alveolar PCO2 was originally 40 mmHg but body temperature increased and CO2 production doubled while no change occurred in alveolar ventilation, what decrease should occur in alveolar PO2 (assume R = 1.0)? A.10 mm Hg B.20 mm Hg C.30 mm Hg D.40 mm Hg E.No change

D •40 mm Hg •Why, alveolar ventilation did not change; PCO2 doubled 40 mm to 80 mm Hg. • •Since PACO2 affects PAO2 therefore PAO2 will decrease by 40

What is obstructive sleep apnea?

Closure of the upper airway during inspiration (obesity, snoring)

1 hr of diving, breathing compressed AIR: -120 ft.-? -150-200 ft.-? -200-250 ft. ? -250 ft.-?

-120 ft.-joviality and increased euphoria -150-200 ft.-drowsiness -200-250 ft. psychomotor disturbances -250 ft.-Narcosis, Coma, Death (8.5 Atm)

how much does pressure increase per feet when divers are going down?

1 Atm pressure will be produced by 33 feet column of water (10.3 m) So if you CALCULATE the 33ft down is 2 atm: Diving at 33 ft. = 2 Atm. of external pressure (1 Atm of air pressure (surface) + 1 Atm of water pressure (submerged))

Decompression Symptoms?

1) 80-90% of individuals develop muscle system pain "Bends" -Bubbles in the tissues 2) 5-10 %-nervous symptoms paralysis and dizziness → Coma -Nitrogen - soluble in the lipid membranes(meaning it can cross BBB) 3) 2% exhibit respiratory system symptoms "Chokes", pulmonary edema and death -Pulmonary extravagation or embolism

hypoxemia vs hypoxia?

Hypoxaemia (or hypoxemia) is an abnormal deficiency in the concentration of oxygen in arterial blood. A frequent error is made when the term is used to describe poor tissue diffusion as in hypoxia. It is possible to have a low oxygen content (eg due to anaemia) but a high PO2 in arterial blood so incorrect use can lead to confusion. Hypoxaemia is different from hypoxia, which is an abnormally low oxygen availability to the body or an individual tissue or organ. The type of hypoxia that is caused by hypoxaemia is referred to as hypoxemic hypoxia. Because of the frequent incorrect use of hypoxaemia, this is sometimes erroneously stated as hypoxic hypoxia.

? is one of the principal causes of death among mountaineers.

Hypoxia

what happens to the A-a gradient with a PE?

Increased

What motor output does the inspiratory center have?

Inspiratory center -> Ventral group -> Phrenic n. -> Diaphragm

Chart of normal respiration and Biot's respiration: -Describe Biot's respiration and when you might see it?

Some type of trauma or stroke can lead to Biot's respiration

Central Chemoreceptors are most sensitive to what?

MOST Sensitive to pH(H+) in CSF!!!!!!!!!!!

mechanisms of nitrogen narcosis?

Nitrogen affects the membrane ionic conductance (neurons and muscle) and this is Caused by the ↑ lipid solubility of nitrogen and as a result it will cross the BBB "Raptures of the Deep"

Where is the inspiratory center?

Dorsal respiratory group (DRG) in medulla

Pharyngitis Pathogenesis?

Either bacterial or viral infection of pharyngeal mucosa •Some pathogens may cause irritation secondary to nasal secretions •Excess secretion and edema and inflammatory cytokine production cause symptoms

What is intrapulmonary shunting when it comes to a PE?

moving blood from one area of the lungs to another so that we do not get full oxygenation of the blood that is coming to the lungs.This is b/c we have a V/Q mismatch. And as a result of the V/Q mismatch we have a greater difference in the PO2 in the alveolus compared to the PO2 in the artery(A-a gradient).

•Ideally V/Q = 1 in all parts of lung, in reality this is about 0.8

ok For pulmonary embolism, we are talking about a flow defect(a defect in Q). So, the ventilation occurs but we don't have flow. Big idea here is V = whatever but Q=0 and so V/Q goes to infinity. V/Q mismatch leads to hypoxemia (low O2 in the blood)

at what pressure in the left atrium will affects of pulmonary edema start to occur?

once you cross about 28mm Hg or left atrial pressure, that pressure is pushed on the capillary vessels in the lungs and that pressure is now hydrostatic pressure and it overcomes that colloid osmotic pressure and contributes to edema by pushing fluid out. So increased hydrostatic pressure in the pulmonary vasculature due to an increase in left atrial pressure. Under normal conditions, left atrial pressure is less than 6 mm Hg, even during strenuous exercise, and compliance of the veins and venules in the pulmonary circulation accommodates increased volume passing through the pulmonary circulation during exercise, so pulmonary artery pressure is minimally affected. When left atrial pressure rises more than 7 mm Hg, the pressure increase is manifested in the pulmonary arterial and capillary pressure. Elevation of capillary pressure above 30 mm Hg is likely to induce pulmonary edema. Edema formation is directly related to left atrial pressure once pulmonary capillary pressure surpasses the colloidal osmotic pressure. The graph above was generated in dogs, where colloidal osmotic pressure is approximately 25 mm Hg. Below this critical value, The lymphatic system is capable of removing the excess exudate. In humans, colloid osmotic pressure is approximately 28 mm Hg, and elevation of left atrial pressure to 28 mm Hg is likely to begin inducing pulmonary edema. Elevation of pulmonary blood pressure for more than two weeks results in expansion of the lymphatic vessels, which combats edema.

In zone 2 what happens with the blood vessels at high lung volumes and at low lung volumes?

opening of the vessels at High lung volumes BUT at low lung volumes these vessels can be prone to collapsing/closing.

What is the Hering-Breuer reflex and how does it work?

The Hering-Breuer inflation reflex, is a reflex triggered to prevent over-inflation of the lungs. (these receptors basically can tell when you have inspired enough air and they tell you to stop taking in more air!) Pulmonary stretch receptors present in the smooth muscle of the airways respond to excessive stretching of the lung during large inspirations. Once activated, they send action potentials through large myelinated fibers of the vagus nerve to the inspiratory area in the medulla and pneumotaxic center of the pons. In response, the inspiratory area is inhibited directly and the apneustic center is inhibited from activating the inspiratory area. This inhibits inspiration, allowing expiration to occur. (pneumotaxic center and the apneustic center are antagonistic to each other.)

What is Apnea?

The absence of spontaneous breathing

Extra info on increased capillary permability

The toxic effects of mustard agent depend on its ability to covalently bind to other substances. The chlorine atom is spiked off the ethyl group and the mustard agent is transferred to a reactive sulphonium ion. This ion can bind to a large number of different biological molecules. Most of all it binds to nucleophiles such as nitrogen in the base components of nucleic acids and sulphur in SH-groups in proteins and peptides. Since mustard agent contains two "reactive groups", it can also form a bridge between or within molecules. Mustard agent can destroy a large number of different substances in the cell by means of alkylation and thereby influence numerous processes in living tissue. The most common cause of death as a result of mustard agent poisoning is complications after lung injury caused by inhalation of mustard agent. Lung injuries become apparent some hours after exposure and will first appear as a pressure across the chest, sneezing and hoarseness. Severe coughing and respiration difficulties caused by pulmonary edema will gradually occur and after a couple of days, a "chemical pneumonia" may develop. Most of the chronic and late effects are also caused by lung injuries.

Prolonged stay at high altitudes causes?

progressive deterioration of mental and motor status

Ventilation Perfusion Mismatch (V/Q mismatch)

•The top of the lung has a higher O2 and the bottom of the lung has higher perfusion. •This will result in a small increase in A-a gradient-this is normal. A small V/Q mismatch is normal due to how the lung is perfused and ventilated. More on this later.

Treatment for Nitrogen narcosis?

Treatment: Slowly ascend (60 ft) - take breaks •Reverse respiration

Prevention of Nitrogen narcosis?

Use helium, control depth NEVER DIVE ALONE Except for helium and probably neon, all gases that can be breathed have a narcotic effect, although widely varying in degree. The effect is consistently greater for gases with a higher lipid solubility, and there is good evidence that the two properties are mechanistically related. As depth increases, the mental impairment may become hazardous. Divers can learn to cope with some of the effects of narcosis, but it is impossible to develop a tolerance. Narcosis affects all divers, although susceptibility varies widely from dive to dive, and between individuals.

"Normal" Ventilation/Perfusion (V'A/Q) Nonuniformity (mismatch)?

take home is that at the base of the lung it is "under-ventilated" and at the apex of the lung it is "Over-ventilated" "Normal" Ventilation/Perfusion (V'A/Q) Nonuniformity (mismatch) Note: Characteristic of upright posture; less important in supine posture 1. higher regions of lungs (apex) get less blood flow than lower (basal) regions Reason: the reduced intravascular pressure leads to partial (Zone 2) or total (Zone 1) vascular compression, thus increasing vascular resistance 2. higher regions of lungs (apex) get less ventilation than lower (basal) regions Reason: In the upright posture, gravity reduces intrapleural pressure in the apical regions compared to the base of the lung. This leads to distension of apical alveoli at rest, thereby reducing apical compliance 3. Ventilation/Perfusion ratio : The effect of gravity on pulmonary circulation is greater than the effect on alveolar ventilation Thus, ventilation/perfusion ratio is less at lung base, so blood flowing through basal region is less well oxygenated 4. In a normal person, nonuniformity is not sufficient to cause a large AaDO2 Note: the tendency of low PA-O2 and high PA-CO2 to increase local pulmonary vascular resistance (vasoconstriction) and decrease local airway resistance (bronchodilation) and vice-versa for the overly ventilated/under perfused regions reduces, but does not necessarily eliminate, the nonuniform V'A/Q http://www.acbrown.com/lung/Notes/RsAaeq/RsAaeqCausNrml.htm

V/Q ratio in zone 3?

the blood flow is much much higher while the ventilation is higher but not as elevated as the blood flow is so the V/Q ratio is decreased.

which zone is blood flow the highest?

zone 3

What does the Pneumotaxic center (Upper pons) do?

•Turns off inspiration (regulates apneustic center) •Limits the burst of action potential in phrenic nerve •Result: Limits the tide of tidal volume and regulates RR(respiratory rate) via the Vagus nerve) •Normal breathing rhythm without this center

How is ventilation measured?

Ventilation (V) is measured as: volume/time

What occurs with a Physiologic Shunt (venous admixture)?

Ventilation to the lungs is absent in the presence of continuing perfusion. •Lungs undergo-hypoxic vasoconstriction- can repair some of physiologic shunt. •Can be caused by mucous plugs, airway edema, foreign bodies, and tumors

What all can influence PVR?

Diverse hormones, neurotransmitters, and inflammatory mediators influence pulmonary blood flow. Of key importance is the O2 and CO2 tensions. Low PAO2 and high PACO2 causes vasoconstriction, which decreases blood flow to poorly ventilated regions of the lung. In contrast, high PAO2 increases perfusion of a region. The mechanism involved in hypoxic vasoconstriction is a depolarization of the vascular smooth muscle cell due to inhibition of Kv, a voltage sensitive potassium channel. Reduction of the K current depolarizes the cell, mobilizing Ca2+. Dont have to know this but read if interested: Neural Sympathetic nerves to larger vessels - NE released appear to increase PVR and decreases distensibility of larger vessels. Parasympathetic - Ach decreases PVR via M3 receptors (endothelium dependent) Humoral Increase PVR: Norepinephrine, alpha adrenergic agonists via a1 receptors, serotonin, prostaglandins F2 and E2, angiotensin, endothelin, alveolar hypoxia (hypoxic pulmonary vasoconstriction), alveolar hypercapnia, low pH of mixed venous blood. Decrease PVR: Acetylcholine, beta adrenergic agonists (b2, endothelium dependent), bradykinin, prostaglandin E1 and I2 (prostacyclin), nitric oxide.

The increase in the partial pressure of oxygen in alveoli causes the increased amount of dissolved oxygen in the water compartment of blood (not bound to erythrocytes) this can lead to ?

Oxygen toxicity

Oxygen toxicity?

Oxygen toxicity: 4 atm = 3040 mm Hg O2 Causes seizures and coma (30-60 min.) Multiple effects: Oxidative stress Damage to alveolar epithelium due to ROS

General Facts about diving pressure changes?

Pressures that affect the diver: Atmospheric pressure + Water column pressure Hyperbarism: ↑ the depth → ↑ in the external pressure (proportionally) Why?? Due to the progressively larger water column High external pressure tends to collapse the alveoli of the lungs The necessity for air to be supplied into the lungs under a higher than external pressure (preventing the lung collapse)

alveolar pCO2 = ?

arterial pCO2

which pressures dominate in zone 2 of the lungs?

arterial pressure >alveolar pressure >venous pressure

which pressures dominate in zone 3 of the lungs?

arterial pressure >venous pressure>alveolar pressure

What is Diffusion limited: ?

as long as a Pp gradient is maintained diffusion will occur along the length of the capillary. 1. Diffusion limited (depends on Graham's law, solubility) e.g. carbon monoxide (CO) CO forms strong bond with Hb => increases in CO content result in very minimal increase in partial pressure => partial pressure difference still exists (ie. equilibrium is not reached) when blood finishes its passage through the alveoli => transfer of CO is limited by the rate of diffusion, not the amount of blood available. once CO crossed capillary- immediately taken up by Hb, so Pp pressure gradient always exists.

Acclimatization to Low PO2: Chronic compensatory effects to hypoxia (why train at altitude?) 7

(Longterm)Results in increased : 1. Pulmonary respiration (O2) 2. pH (blowing off more CO2)(have respiratory alkalosis) 3. Number of RBCs (Carrying capacity of O2) 4. Diffusing capacity of the lungs 5. Vascularization of peripheral tissues(it stimulates angiogenesis) 6. Utilization of O2 (Despite hypoxia (Mitochondria more efficient and increase #) 7. Increased synthesis of 2,3-DPG (glycolysis more efficient)

What is Minute Ventilation (VE)?

(VE) = volume you ventilated in a minute (with the dot over it means minute)

Biot's Respiration: -What is it? -prognosis? -what causes it biochemically? -example of something that could cause it?

-Abnormal pattern of breathing characterized by groups of quick, shallow inspirations followed by regular or irregular periods of apnea. -It generally indicates a poor prognosis. -Biot's respiration is caused by damage to the pons due to strokes or trauma or by pressure on the pons.; It can also be caused by opioid use.

Allergic Conjunctivitis: -Pathogenesis? -Presentation?

-Pathogenesis •Same as allergic rhinitis -Presentation •Ocular itching, burning, redness, conjunctival and/or eyelid edema, tearing •Symptoms are usually bilateral

-What is central sleep apnea? (aka congenital central hypoventilation syndrome (CCHS) or primary alveolar hypoventilation) Ondine's curse) -Is there presence of respiratory effort?

-Cessation of ventilatory drive to respiratory muscles -NO

-What happens with Obstructive Sleep apnea? -Is there presence of respiratory effort?

-Closure of the upper airway during inspiration (obesity, snoring) -YES

Sinusitis: -Differential diagnosis? -Treatment for acute sinusitis? •Viral:? •Bacterial? -Environmental control?

-Differential diagnosis •Common cold, allergies, facial pain, headache, dental pain -Treatment for acute sinusitis •Viral: symptomatic management •OTC analgesics and antipyretics, saline irrigation, decongestants, intranasal glucocorticoids •Bacterial •Symptomatic management (same as viral) •Observation for 7 days, antibiotics if no improvement -Environmental control •Wash hands, get recommended vaccines, avoid environmental triggers, use a humidifier

Pharyngitis: -Differential diagnosis? -Treatment? -Environmental control?

-Differential diagnosis •Rhinitis/sinusitis, GERD, trauma, irritation or drying of the pharynx, chemical exposure, referred pain -Treatment •Symptom control: OTC analgesics, throat lozenges or sprays •Antibiotics for bacterial infections -Environmental control •Avoid exposure to irritants, use humidifier, general hygiene to avoid illness

Pharyngitis: -Epidemiology?

-Epidemiology •1-2% of all annual US ambulatory care visits •Incidence peaks in childhood/adolescence

Allergic Conjunctivitis: -Epidemiology?

-Epidemiology •>20% of population annually •Incidence is increasing •**Average age of onset: 20 years**

Croup (laryngotracheitis): -Epidemiology?

-Epidemiology •Most common in children 6 months-3 years old •More common in males •Family history is a risk factor •Most cases in fall, winter

Rhinitis: -Epidemiology? -Presentation?

-Epidemiology •Virtually everyone will experience at some point -Presentation •One or more: Sneezing, rhinorrhea, nasal itching, nasal congestion, cough •Most common forms: allergic rhinitis, nonallergic rhinitis, atrophic rhinitis, rhinitis of pregnancy, occupational rhinitis

Tonsillitis Epidemiology?

-Epidemiology •~1-2% of outpatient visits •More common in winter, early spring •Viral in kids <5 years old •GAS: 5-15% of adults, 15-30% of 5-15 year olds

The Common Cold (Rhinosinusitis): -Etiopathogenesis? -Epidemiology? -Presentation?

-Etiopathogenesis •More than 200 subtypes of viruses •Most capable of reinfection after reexposure -Epidemiology •Most frequent acute illness in the industrialized world •Higher incidence in men; highest in adults 45-64 years old •Seasonality •Fall, late spring: rhinoviruses, parainfluenza, influenza viruses •Winter, spring: coronaviruses, RSV •Enteroviruses: year round, but most often in summer •Adenoviruses: not seasonal; barracks, daycares, hospitals -Presentation •Nasal congestion, rhinorrhea, sneezing, sore throat, cough, low grade fever, headache, malaise

Sinusitis: -Etiopathogenesis?

-Etiopathogenesis •Viral (rhinovirus, influenza, parainfluenza) •Inflammation causes transudation of fluid into nasal cavity and sinuses •Cytotoxicity on nasal cilia impairs mucociliary clearance •Mucosal edema, lots of secretions, and ciliary dyskinesia lead to obstruction •Bacterial (S. pneumoniae, H. influenzae, M. catarrhalis) •Secondary infection; mucus allows bacterial overgrowth •Biofilms are common in chronic bacterial sinusitis •Fungal (Aspergillus spp., Fusarium spp., Mucorales spp., dematiaceous molds) •Most commonly in immunocompromised patients Hyphal invasion of blood vessels results in tissue infarction

How does Decompression Sickness - (Ascending Rapidly) work?

-Increased external pressure = increased amount of gas to be dissolved in fluid (blood) -Rapid ascension causes a development of nitrogen bubbles in blood -The bubbles form in the tissues and block the blood vessels Physics: ↑ Pressure - ↑ amount of the dissolved gas in the solution Sudden ¯ in the external pressure results in the escape of the gases from a solution

Allergic Conjunctivitis: -Lab tests? -Differential diagnosis?

-Lab tests •Clinical diagnosis •Possibly refer to ophthalmologist -Differential diagnosis •Infectious conjunctivitis, dry eye, blepharitis, toxic conjunctivitis, episcleritis/scleritis, keratitis, ocular rosacea, keratoconjunctivitis

Sinusitis: -Lab tests?

-Lab tests •Clinical diagnosis •Viral vs bacterial based on duration and progression of symptoms •Imaging and micro testing are reserved for patients with suspected complications

Allergic Rhinitis: -Lab tests? -Differential diagnosis?

-Lab tests •Diagnosis is clinical •Allergy skin or serum tests confirm sensitization -Differential diagnosis •Causes of nasal obstruction •GERD •Nasal tumors •CSF rhinorrhea

The Common Cold (Rhinosinusitis): -Lab tests? -Differential diagnosis?

-Lab tests •Diagnosis is clinical •Flu tests (viral PCR) -Differential diagnosis •Allergic/seasonal rhinits, bacterial pharyngitis/tonsillitis, acute bacterial rhinosinusitis, influenza, pertussis

Tonsillitis: -Lab tests? -Differential diagnosis?

-Lab tests •Rapid antigen test or throat culture -Differential diagnosis •Peritonsillar abscess (quinsy), Lemierre syndrome, epiglottitis, Ludwig's angina, tonsillolith

Croup (laryngotracheitis): •Lab tests •Differential diagnosis •Treatment •Environmental control

-Lab tests •Usually not necessary, diagnosis is clinical -Differential diagnosis •Epiglottitis, foreign body, allergic reaction, airway anomalies -Treatment •Airway assessment, supplemental O2, inhaled bronchodilator, antibiotics for bacterial infection -Environmental control •Vaccination, general hygiene

Acute effects of high altitude on unacclimatized person without an oxygen apparatus. -12,000 ft? -18,000 ft? -23,000 ft?

-Mental and muscle fatigue, nausea, euphoria. -Twitching/Seizures -Coma→Death

Allergic Rhinitis Pathogenesis?

-Pathogenesis(type 1 hypersensitivity) •T cell-dependent allergen-specific IgE production •IgE binds to Fc receptors on mast cells (sensitization) •Mediated by Th2 cells and cytokines -Immediate response •Vascular and smooth muscle reactions due to mast cells •Late-phase inflammatory reaction Immediate hypersensitivity diseases are initiated by the introduction of an allergen, which stimulates IL-4-producing helper T cell responses and IgE production. IgE sensitizes mast cells by binding to FcεRI, and subsequent exposure to the allergen activates the mast cells to secrete the mediators that are responsible for the pathologic reactions of immediate hypersensitivity.

Croup (laryngotracheitis): -Presentation?

-Presentation •Barking cough, fever, stridor, dyspnea, odynophagia •Radiograph may show steeple sign •Severity assessed with Westley croup score

Sinusitis: -Presentation?

-Presentation •Facial pain/pressure, congestion, nasal obstruction, nasal/postnasal purulence, hyposmia, fever •PE: erythema or edema over cheekbone, tenderness with percussion

Decompression and treatment of bends?

-Pressurized tank: _Diver returned to the original pressure = equal to the previous depth _Slowly decompressed using the pre-assigned tables _Repeated several times

Allergic Rhinitis: -Treatment? -Environmental control?

-Treatment •Oral antihistamines (cetirizine, loratadine, fexofenadine, desloratadine, levocetirizine) •Glucocorticoid nasal sprays (beclomethasone, flunisolide, budesonide, fluticasone, etc) •Immunotherapy (shots or sublingual tablets) -Environmental control •Allergen avoidance

Tonsillitis: -Treatment? -Environmental control?

-Treatment •Supportive care (analgesia, hydration) •Antibiotics for bacterial infection •Penicillins for GAS -Environmental control •Tonsillectomy is an option in patients with recurrent infections •Avoid exposure to irritants, use humidifier, general hygiene to avoid illness

The Common Cold (Rhinosinusitis): -Treatment? -Environmental control?

-Treatment •Symptomatic therapy: Tylenol, NSAIDs, antihistamine/decongestants, expectorants -Environmental control •Hand washing, sneeze into elbows •Disinfect surfaces

Laryngitis -Treatment? -Environmental control?

-Treatment •Voice rest, steam inhalation -Environmental control •Avoid irritants, dietary modification for GERD

Allergic Conjunctivitis: -Treatment (topical)? -Environmental control?

-Treatment (topical) •Vasoconstrictor/antihistamine combos (naphazoline, pheniramine) •Antihistamine/mast cell stabilizing combos (olopatadine, alcaftadine, bepostastine, azelastine, cetirizine, ketotifen, emedastine) •Mast cell stabilizers (cromolyn sodium, nedocromil, iodoxamide tromethamine, pemirolast) •Glucocorticoids (short term) -Environmental control •Allergen avoidance •Eye care

-which zone is blood flow the lowest? -why?

-Zone 1 -The high alveolar pressure compresses the capillary and reduce blood flow in zone one.

3 drugs that can treat Acute Mountain Sickness?

1. Acetazolamide(carbonic anhydrase inhibitor) 2. Inhaled NO 3. Sildenafil

7 Risk Factors for PE?

1. Alterations in blood flow: 2. immobilization (after surgery, injury or long-distance air travel) 3. pregnancy (also procoagulant) 4. obesity (also procoagulant) 5. Estrogen-containing hormonal contraception 6. Genetic thrombophilia (factor V Leiden, prothrombin mutation, protein C deficiency, protein S deficiency, antithrombin deficiency, hyperhomocysteinemia and plasminogen/fibrinolysis disorders). 7. Smoking

What are the 2 major problems with general anesthesia on respiration?

1. Causes depression of respiratory centers and muscles 2. Alters gas exchange

The Common Cold (Rhinosinusitis): Common Cold Therapies? 4

1. Cromolyn sodium and ipratropium bromide (nasal sprays) 2. Dextromethorphan: cough suppressant 3. Phenylephrine/pseudoephedrine: decongestant 4. Guaifenesin: expectorant

2 other names for The Bends?

1. Decompression Sickness (DCS) 2. Caisson Disease

Regulator of Blood Flow/PVR: List of Vasodilators? 5

1. High PAO2 2. Inhaled Nitric Oxide* 3. Sympathetic EPI.; α2,β2-adrenergic 4. PGE1, PGI2*(prostaglandins) 5. Bradykinin

Ventilatory drive or ventilatory response to changes in Pco2 can be reduced by? 3

1. Hyperventilation 2. Drugs (morphine, barbiturates, and anesthetic agents) 3. Increased work of breathing (COPD)

Respiratory Responses to Exercise: -O2 consumption? -vent rate? -arterial PO2 and PCO2? -Arterial pH? -Venous PCO2? -V/Q? -O2 Hb dissociation curve?

1. O2 consumption increase ≈ 15X 2. Ventilation rate increase ≈ 15X 3. Arterial PO2 and PCO2 no change 4. Arterial pH no change 5. Venous PCO2 increase 6. V/Q approaches 1.0 (evenly matched)(during exercise all 3 lung zones approach a V/Q of 1. 7. O2 hemoglobin dissociation curve-shift to the right (2,3 DPG)

6 Causes of Hypoxia?

1. Hypoxemia (PO2 has fallen below 60 mmHg) Def. to know 2. Decreased cardiac output (CO) (↓ blood flow) 3. Hypoxemia (↓PaO2 cause, ↓ % O2 sat.) 4. Anemia (↓ Hb causes ↓ O2 content) 5. CO poisoning (↓ O2 content) 6. Cyanide poisoning Hypoxia is a generalized hypoxia, an inadequate supply of oxygen to the body as a whole. The term "hypoxemic hypoxia" specifies hypoxia caused by low partial pressure of oxygen in arterial blood. In the other causes of hypoxia that follow, the partial pressure of oxygen in arterial blood is normal. Hypoxemic hypoxia may be due to: •Low partial pressure of atmospheric oxygen such as found at high altitude or by replacement of oxygen in the breathing mix either accidentally as in the modified atmosphere of a sewer or intentionally as in the recreational use of nitrous oxide. • Pulmonary shunt by a decrease in oxygen saturation of the blood caused by sleep apnea or hypopnea • Diffusion impairment Inadequate pulmonary ventilation (e.g., in chronic obstructive pulmonary disease or respiratory arrest). •Shunts in the pulmonary circulation or a right-to-left shunt in the heart. Shunts can be caused by collapsed alveoli that are still perfused or a block in ventilation to an area of the lung. Whatever the mechanism, blood meant for the pulmonary system is not ventilated and so no gas exchange occurs (the ventilation/perfusion ratio is zero). Normal anatomical shunt occurs in everyone, because of the Thebesian vessels which empty into the left ventricle and the bronchial circulation which supplies the bronchi with oxygen.

5 major Causes of Pulmonary Edema?

1. Increased capillary hydrostatic pressure(increased pressure that pushes fluid out of capillariesa) 2. Decreased colloid osmotic pressure(decreased pressure that pulls fluid back into caps) 3. Increased capillary permeability 4. Decreased interstitial pressure 5. Lymphatic insufficiency

Ways to haveLymphatic Insufficiency which end up causing pulmonary edema?

1. Increased central lymphatic pressure 2. Blockage of lymph drainage (can be a tumor) Acute lymphangitis affects a critical member of the immune system--the lymphatic system. Waste materials from nearly every organ in the body drain into the lymphatic vessels and are filtered in small organs called lymph nodes. Foreign bodies, such as bacteria or viruses, are processed in the lymph nodes to generate an immune response to fight an infection. In acute lymphangitis, bacteria enter the body through a cut, scratch, insect bite, surgical wound, or other skin injury. Once the bacteria enter the lymphatic system, they multiply rapidly and follow the lymphatic vessel like a highway. The infected lymphatic vessel becomes inflamed, causing red streaks that are visible below the skin surface. The growth of the bacteria occurs so rapidly that the immune system does not respond fast enough to stop the infection. If left untreated, the bacteria can cause tissue destruction in the area of the infection. A pus-filled, painful lump called an abscess may be formed in the infected area. Cellulitis, a generalized infection of the lower skin layers, may also occur. In addition, the bacteria may invade the bloodstream and cause septicemia. Lay people, for that reason, often call the red streaks seen in the skin "blood poisoning." Septicemia is a very serious illness and may be fatal.

Ways to have Increased Capillary Permeability which end up causing pulmonary edema? 5

1. Inhaled or circulating toxins (chlorine, sulfur dioxide, nitrogen oxide) 2. Radiation 3. Oxygen toxicity 4. ARDS 5. inflammation Destruction of the capillary endothelium allows protein to get into interstitium or anything increases permeability -i.e. inflammation

Allergic Rhinitis 3 types?

1. Intermittent(symptoms happen to certain exposures like a cat's hair) 2. Seasonal 3. Persistent/perennial

Regulator of Blood Flow/PVR: List of Vasoconstrictors? 7 (bold are most important)

1. Low PAO2 hypoxic vasoconstriction 2. High PACO2 3. Angiotensin II 4. Parasympathetic M3 5. Sympathetic NE/α1 6. Endothelin (Use of Endothelin antagonist is used to treat pulmonary HTN) 7. Serotonin

Acute effects of zero gravity? 2

1. Motion Sickness (50% of astronauts) 2. Translocation of fluids within the body (No Gravity - bloating)

Ways that you get Increased Capillary Hydrostatic Pressure that causes pulmonary edema? 3

1. Myocardial infarction (i.e. left ventricular failure increases wedge pressure) 2. Mitral stenosis 3. Fluid overload (infusion of saline, plasma or blood raising pulmonary capillary pressure) Pressure in cap increase, so flow out

Ways to have Decreased Colloid Osmotic Pressure which end up causing pulmonary edema? 3

1. Over transfusion of saline(diluting out the concentration of proteins you have in the plasma) 2. Hypoalbuminemia (liver disease) 3. Renal disease - loss of proteins Decrease in plasma proteins = loss of colloidal pressure

How do we control for the adverse affects of general anesthesia on respiration? 2

1. Preoxygenation • The utilization of 80% oxygen during the induction phase of anesthesia which Raises FRC enough to prevent atelectasis 2. Utilization of Continuous positive airway pressure (CPAP) + Preoxygenation • Air blown into the lungs under higher pressure(basically increases the pressure within the alveoli so that it helps keep them inflated. • Keeps the alveoli open ( intra-alveolar pressure) • Utilized in morbidly obese patients

Ways to have Decreased Interstitial Pressure which end up causing pulmonary edema? 3

1. Rapid removal of pleural effusion 2. Pneumothorax 3. Hyperinflation

What happens to the airways in Anesthesia?

1. Reduction of FRC below the threshold (aka - closing volume) 2.decrease in elastic recoil 3. decrease negative pleural pressure Result: Closure of small airways and alveoli - Atelectasis

What are 4 major sites involved in a control of respiration?

1. Respiratory control center (RCC) •Brain stem (medullary respiratory centers, pontine centers) Feedback: (things that sense changes and send that info to the RCC) 2. Central chemoreceptors (most important) • Surface of the medulla - Cerebrospinal fluid(they sense changes in the CSF) 3. Peripheral chemoreceptors • Carotid and Aortic bodies - Blood 4. Mechanoreceptors in lungs and joints Also, voluntary control can also originate for the Cerebral cortex. It temporarily overrides the brain stem respiratory centers •Breathing during swallowing process, can also hypo and hyperventilate, but will eventually have to correct. we can temporarily override our innate sense to breath. we can make ourselves hyperventilate and we can hold our breath.

Pulmonary Artery Pressure in Exercise: -All but a small percentage of the cardiac output passes through the pulmonary circulation. Thus, in exercise, as cardiac output increases, so does the flow through the pulmonary circulation. Yet, pulmonary pressure does not increase proportionally. What are the two reasons for this?

1. The pulmonary vessels are distensible, and the volume of each vessel can increase up to 2-fold. 2. The number of capillaries that are open increases, which can increase the volume of pulmonary circulation up to 3-fold. Keeping pulmonary pressure low reduces the work of the right heart and the formation of pulmonary edema.

2 kinds of sleep apnea?

1. central 2. obstructive

Chronic effects of zero gravity? 5

1. decreases Baroreceptor sensitivity 2. decreasesCardiac output and heart work 3. decreases Bone density (decreases calcium and phosphates in the blood through the kidneys) 4. decreases Muscle mass, strength and work capacity → atrophy 5. Fainting astronauts: Reduced orthostatic tolerance on earth(have symptoms when standing that are relieves when sitting down)

Five Causes of Hypoxemia?

1. high altitude 2. hypoventilation 3. diffusion defect 4. V/Q defect 5. right to left shunt

What is a normal A-a gradient?

10 mm Hg

pressure in right ventricle

25/0 mmHg

What is Central sleep apnea?

A genetic condition that alters your drive to breath.

What do lymphatics do in lungs?

A lymphatic system returns fluid and plasma protein that escapes the pulmonary and bronchial circulations back to the circulatory system, thereby guarding against edema formation.

What is Pulmonary Vascular resistance?

A term used to define the resistance to flow that must be overcome to push blood through the pulmonary vascular system.

How to diagnose respiratory failure when Hypoxia is present and the first test you do is calculating the A-a gradient?

A-a gradient = PAO2 - PaO2 Normal A-a gradient = (Age+10) / 4 A-a gradient (Alveolar to arterial gradient): Provides an assessment of alveolar-capillary gas exchange. To calculate you need the alveolar PO2 (PAO2) and arterial pO2 (paO2). The larger the gradient, the more serious the respiratory compromise. The alveolar-arterial PO2 difference (AaDO2) is used to diagnose the existence of a shunt. In the absence of shunts and with adequate ventilation and perfusion, PAO2 should equal PaO2. As unoxygenated blood is mixed with the pulmonary vein blood, the difference between PAO2 and PaO2 increases in proportion to the amount of blood that is shunted around the lungs. Given the normal dilution of arterial O2 by the bronchial and coronary circulation, the A-aDO2 is expected to be approximately 10 mm Hg. AaDO2 greater than 25 indicates a shunt which further diluting the pulmonary capillary PO2.

What is Apneusis?

Abnormal breathing with prolonged inspiratory gasps followed by brief expiratory movement

What all occurs with Acute Mountain Sickness?

Acute Pulmonary Edema Persistent cough bringing up white, watery, or frothy fluid which can lead to A feeling of impending suffocation at night -Cheyne-Stokes Breathing 1.Hypoxia-induced constriction of pulmonary capillaries in some areas of the lungs (hypoventilated areas) 2.Vasoconstriction increases the hydrostatic pressure in lung capillaries 3.Increased hydrostatic pressure causes the leakage of fluid out of the vasculature (including cerebral edema) 4.Fluid accumulates in the interstitial space and in the alveoli

Effects each has on PaO2 and A-a gradient -high altitude -hypoventilation -diffusion defect -V/Q defect -right to left shunt

Alveolar hypoventilation If the alveolar ventilation is low, there may be insufficient oxygen delivered to the alveoli each minute. This can cause hypoxemia even if the lungs are normal, as the cause may be outside the lungs (e.g., airway obstruction, depression of the brain's respiratory center, or muscular weakness). Low inspired oxygen partial pressure (low PiO2) If the partial pressure of oxygen in the inspired gas is low, then a reduced amount of oxygen is delivered to the gas exchanging parts (alveoli) of the lung each minute. The reduced oxygen partial pressure can be a result of reduced fractional oxygen content (low FiO2) or simply a result of low barometric pressure, as can occur at high altitudes. This reduced PiO2 can result in hypoxemia even if the lungs are normal Shunt Shunting of blood from the right side to the left side of the circulation (right-to-left shunt) is a powerful cause of hypoxemia. The shunt may be intracardiac or may be intrapulmonary. It has been traditionally thought that this cause could be readily distinguished from the others as the only cause that cannot be corrected by the administration of 100% oxygen. Ventilation-perfusion inequality Ventilation-perfusion inequality (or ventilation perfusion mismatch) is a common cause of hypoxemia in people with lung disease. It is the areas of the lung with ventilation/perfusion ratios that are less than one (but not zero) that cause hypoxemia by this mechanism. A ventilation/perfusion ratio of zero is considered a shunt. Impaired diffusion Impaired diffusion across the blood-gas membrane in the lung can cause hypoxemia. However, this is a very rare cause as it is only in extremely unusual circumstances that actually does cause a problem. Most of the past cases once thought to be due to a diffusion problem are now recognized as being due to ventilation-perfusion inequality.

What are J receptors?

Alveolar walls-sense increase in blood or fluid filling stimulate more breathing Now for J receptors, they are short for juxtacapillary so they sit right next to the capillaries on our lungs. They sense increased blood or fluid, so they get activated in edema, pneumonia, congestive heart failure (or just increased blood flow) with this increased fluid, you gotta think you need to oxygenate it more. Finally, these receptors have been found in the walls of bronchi, the larynx, and the nose, they appear to be part of a widespread population of nociceptors found in most tissue. For this reason, they are often referred to as pulmonary C-fiber receptors. they can be activated with exercise.

What occurs with a Right to Left Shunt (Anatomic Shunt)?

Anatomic shunt occurs when venous blood bypasses the gas exchange and goes directly into arterial blood. (ex. In the heart defect). Most anatomic shunts are right to left shunts that occur in the heart where when deoxygenated blood from the right atrium or ventricle crosses the septum and mixes with blood form the left atrium or ventricle The effect of this right to left shunt is to mix deoxygenated blood with oxygenated blood and results in varying degrees of arterial hypoxemia.

If the person in the above question has emphysema which caused his PaO2 to be 60 mm Hg, his A-a gradient would be: A. 60 mm Hg B. 30 mm Hg C. 20 mm Hg D. 10 mm Hg E. Impossible to determine with the given information

Ans: B (90 - 60 = 30 mmHg) and remember that an A-a gradient greater than 25 mmHg means that you have impaired gas exchange.

A man breathing room air at sea level has an alveolar ventilation of 2 L/min. The blood gases show a PaCO2 of 48 mm Hg and a PaO2 of 70 mm Hg. The alveolar oxygen tension (PAO2) is: A.140 mm Hg B.110 mm Hg C.100 mmHg D.90 mm Hg E.60 mm Hg

Ans: D PAO2= 150 - 48/.8 = 90

A 72-year-old woman who recently underwent hip replacement surgery develops a large left lower lobe pulmonary embolus. The ventilation and perfusion status in the alveoli of her affected lobe could best be described by which of the following? A.VA is 0, Q is normal B.VA is 0, Q is low C.VA is normal, Q is high D.VA is normal, Q is normal E.VA is normal, Q is 0

Ans: E during a PE ventilation will be normal and blood flow will be 0

Which part of the lung is "Over-ventilated" and represents physiological dead space?

Apex where there is high PO2 and low PCO2

So sum up what the 2 centers in the pons do?

Apneustic center tells you to breath in longer (positive feedback) and the Pneumotaxic center(negative feedback) tells you to stop inhaling.

What are the Extra-alveolar vessels?

Arteries, arterioles, vein, venules outside of the alveolar wall

Normal Capillary Fluid Balance?

As in other capillary beds, the balance of fluid across the alveolar capillaries is a function of the balance between the oncotic and hydrostatic pressures. Under normal conditions, there is a small outward driving force for fluid to leave the pulmonary capillaries and enter the interstitial space. This fluid, however, does not normally enter the alveoli and and accumulate in the airspace, since the interstitial pressure is normally negative relative to the atmosphere. Pores in the alveolar epithelium thereby provide a pathway by which fluid on the surface of the alveoli is "sucked" into the interstitial space, keeping the alveoli dry.

Effect of vital capacity on total pulmonary vascular resistance:

As lung volume increases the pressure on the alveoli compresses the capillary vessels and as a result their vascular resistance increases as we increase lung volume. The opposite is true for the extra-alveolar vessels; at high lung volumes the extra-alveolar vessels are pulled open due to the recoil forces. The result is perfusion is most optimal for the pulmonary vasculature at or near the FRC!

With general anesthesia if your FRC is less than your closing volume this will contribute to ?

Atelectasis, With anesthesia you have a decrease in the FRC which will decrease it below the closing volume

why is pH lower and bicarb higher in venous blood?

B/c of metabolically active tissue converting CO2 to bicarb and H+.

Central Chemoreceptors work how?

BBB is pretty impermeable to H+ and HCO3- But.......... •CO2 diffuses easily out of caps •In CSF forms H+ and HCO3- •H+ diffuses out of CSF to medulla and binds central chemoreceptors and stimulates breathing

Laryngitis bacterial Etiopathogenesis?

Bacterial superinfection may occur; usually 7 days after symptoms begin (S. pneumoniae, H. influenzae, M. catarrhalis)

Tonsillitis bacterial Etiopathogenesis?

Bacterial: S. pyogenes, S. aureus, S. pneumoniae, H. influenzae

Which part of the lung represents a physiological shunt and is "Under-ventilated"?

Base where there will be Low PO2 and relatively high pCO2

How to we control the volume of air inspired and expired?

By controlling: •Frequency of breaths (RR) •Tidal volume (TV)

During exercise, the limiting factor for oxygen delivery to the muscles will be?

Cardiac Output. Different gases have different solubility factors, and some are insoluble. Gases that are insoluble in the blood do not chemically combine with proteins in the blood and equilibrate rapidly between alveolar gas and blood. The diffusion of insoluble gases between alveolar gas and blood is considered perfusion limited because of the partial pressures of gas leaving the capillary has reached equilibrium with alveolar gas and is limited by the amount of blood perfusion in the alveolus. In contrast, a diffusion limited gas such as CO has low solubility in the alveolar capillary membrane but high solubility in the blood because of its high affinity for hemoglobin. These features prevent the equilibration of CO between alveolar gas and blood during the red blood cell transit time. The high affinity for CO with Hb enables large amounts of CO to be taken up in the blood with little or no appreciable increase in its partial pressure. Blood enters the arterial end of the pulmonary capillary at a PO2 of 40 mm Hg, whereas alveolar PAO2 is approximately 100 mm Hg. As the blood passes along the capillary, O2 diffuses across the blood gas barrier and dissolves in the plasma, increasing the plasma PO2 until it equals PAO2. Under normal conditions, equilibration occurs before the midpoint of the capillary. In other words, all the O2 that will bind the Hb happens at the beginning of the capillary system, so if you increase perfusion during exercise, you will generally still bind nearly all of your Hb with O2. If you increase in perfusion, you do not compromise PaO2. So, in exercise (the limiting factor for oxygen delivery to the muscles will be cardiac output).

Shallow Water Blackout causes and dangerous facts?

Cause: §Hyperventilation initially decreases the CO2 in the blood §Low CO2 does not reach threshold on time to indicate drowning Dangerous Facts: •CO2 is the main determinant of respiratory drive •The CO2 levels are too low to signal drowning (CO2 blown out by initial hyperventilation) leads to Brain Ischemia and thus loss of consciousness.

Cerebral Cortex can temporarily override automatic brain stem centers: What happens when you hypoventilate?

Causes a decrease in PaO2 + Increase in PaCO2 Both are STRONG drives for ventilation

What is the major way in which breathing is controlled?

Central Chemoreceptors

Biot's respiration can be similar to ?

Cheyne-Stokes respiration (but CSR will have increased amplitude and frequency)

Pontine Centers Apneustic and Pneumotaxic Centers control what?

Controls the action of Inspiratory center

What is a Single photon emission computed tomography (SPECT, or less commonly, SPET)?

Coronal slices of a ventilation/perfusion lung scan (SPECT): while the ventilation (A) normal ventilation (B) flow is not seen in lower right lung. Diagnosis: mismatch defect of ventilation and perfusion caused by pulmonary embolism The test you order: A lung scan using radioactive albumin and radioactive xenon (or something else to compare ventilation and perfusion) Single photon emission computed tomography (SPECT, or less commonly, SPET) is a nuclear medicine tomographic imaging technique using gamma rays. It is very similar to conventional nuclear medicine planar imaging using a gamma camera. However, it is able to provide true 3D information. This information is typically presented as cross-sectional slices through the patient, but can be freely reformatted or manipulated as required. The basic technique requires injection of a gamma-emitting radioisotope (also called radionuclide) into the bloodstream of the patient. Occasionally the radioisotope is a simple soluble dissolved ion, such as a radioisotope of gallium(III), which happens to also have chemical properties which allow it to be concentrated in ways of medical interest for disease detection. However, most of the time in SPECT, a marker radioisotope, which is of interest only for its radioactive properties, has been attached to a special radioligand, which is of interest for its chemical binding properties to certain types of tissues. This marriage allows the combination of ligand and radioisotope (the radiopharmaceutical) to be carried and bound to a place of interest in the body, which then (due to the gamma-emission of the isotope) allows the ligand concentration to be seen by a gamma-camera.

Cerebral Cortex can temporarily override automatic brain stem centers: What happens when you hyperventilate?

Cortex overrides breathing center which leads to a decrease in PaCO2 and an increase in arterial pH which will decrease/disrupt your normal breathing pattern.

What occurs with Kussmaul Breathing?

Deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA), but also renal failure. •Hyperventilation, which is any breathing pattern that reduces carbon dioxide in the blood due to increased rate of respiration. •In metabolic acidosis, breathing is first rapid and shallow but as acidosis worsens, breathing gradually becomes deep, labored and gasping.

High Altitude Complications: symptoms?

Fatigue, dizziness, breathlessness, headaches, insomnia, malaise, nausea, vomiting, body pain, loss of appetite, ear-ringing, blistering and purpling of the hands and feet, and dilated veins.

Where are the irritant receptors of the lungs located

In epithelial cells of the airways

What is a Pulmonary Embolism (PE)?

Is a blockage of the pulmonary artery (or one of its branches), usually when a venous thrombus (blood clot from a vein), becomes dislodged from its site of formation and embolizes to the arterial blood supply of one of the lungs. This process is termed thromboembolism.

Chart with Kussmaul and Cheyne-Stokes respiration and description of both with examples of what each cause?

Kussmaul breathing is due to some kind of metabolic issue.

What does elevated pulmonary artery pressure lead to?

Leads to dilated pulmonary arteries which leads to the right side of the heart working harder tp pump blood to the lungs and thus they can enlarge/hypertrophy

Where are the Peripheral Chemoreceptors?

Located in carotid bodies at bifurcation of common carotid arteries and aortic bodies above aortic arch

Central Chemoreceptors are located near what 2 nerves?

Located near CN IX and CNX A short distance from DRG

What is the definition of Shallow Water Blackout?

Loss of consciousness in divers at depths less than 15 ft

•Ventilation (V) - ?

Measured as the frequency of breathing multiplied by the volume of each breath (tidal volume)

How do Lung stretch receptors work?

Mechanoreceptors - initiate a Hering-Breuer reflex. Acts to ↓ depth of inspiration (plays only minor role in humans)

minute ventilation, alveolar ventilation and oxygen alveolar ventilation normal values?

Minute vent: 6 L/min Alveolar ventilation: 4.8 L/min ventilation of the alveoli with oxygen can be calculated. Therefore, alveolar O2 ventilation is approximately 1.0 L/min. This represents the amount of O2 being delivered to the alveoli and is available for exchange with blood in the alveolar capillaries.

Can giving 100% O2 for an Anatomic shunt help return pO2 back to normal?

NO! One important feature in an Anatomic shunt is when giving a person 100% O2, the blood that bypasses the lung never gets O2 and since the hemoglobin will be saturated already, the extra O2 added is in the form of dissolved O2.

What is happenings with the phrenic nerve and the diaphragm due to the Inspiratory center?

Nerve : 1.Period of quiescence 2.Burst of action potentials 3.Back to quiescence Diaphragm : 1.Period of quiescence (no contraction) 2.Burst of action potentials = Contraction 3.Back to quiescence (no contraction)

Laryngitis Non-infectious Etiopathogenesis?

Non-infectious: vocal trauma, allergy, GERD, asthma, pollution, smoking

Averages: Normal Cardiac output =? Normal PAP=? Mean LAP=?

Normal Cardiac output =5 L/min Normal PAP=15 mm Hg Mean LAP=6 mmHg

What is a normal PVR in both mm Hg and Wood unit?

Normal PVR = 1 mm Hg/(l/min) or Wood unit 79.5 dyne • sec • cm-5

Cardio/Pulmonary Circulation (Closed loop)

Okay, so you should know by now that the circulatory system is a closed loop, that all the blood from the heart goes through the lungs where it gets oxygenated. Pulmonary veins carry oxygenated blood to the heart and they to the systemic vasculature. Now since the right heart only has to pump to the lungs the pressures that the right heart generate are much smaller than the left heart. Finally, the pulmonary capillaries are very delicate with low pressures entering them and if you increase the resistance in them, they can become leaky (this results in pulmonary edema).

PVR equation

PVR = PAP - LAP ÷ CO

Info on PVR:

PVR can be estimated using a form of Ohm's Law, such that PVR equals the difference in pressure between the pulmonary artery and left atrium, divided by the cardiac output. The units are mm Hg/(l/min), which is also called a Wood unit. A Wood unit can be converted to dyne ∙sec ∙cm-5 by multiplying by 79.9. Normal pulmonary vascular resistance is approximately 1 mm Hg/L/min, compared to a normal peripheral vascular resistance of 20 to 40 mm Hg/L/min. However, it should be remembered that the pulmonary vasculature is not composed of rigid tubes, but rather the vessels are distensible and therefore flow and resistance do not change in a linear fashion as pulmonary artery pressure increases. Furthermore, PVR changes with lung volume, which is not reflected in the equation. Thus, a change in the calculated PVR does not automatically equate to a change in the actual PVR.

PaCO2 change ® Sensed by ?

PaCO2 change ® Sensed by BOTH the central and peripheral receptors® Medullary respiratory center ® Regulation of minute ventilation

Is N2O perfusion or diffusion limited?

Perfusion limited. N2O (Nitrous oxide) does not bind any Hb(its only place to go is into the plasma) so it reaches equilibrium pretty quick, because it diffuses pretty easily so the only way to get more N2O in the blood is to remove the saturated blood (so we say N2O is perfusion limited). => increase in N2O content results in rapid rise in partial pressure (equilibrium within 0.075 second) => equilibrium is reached very early on => transfer of N2O is limited by the amount of blood available. O2 only becomes diffusion limited in Fibrotic diseases and strenuous exercise.

Dan Hsieh celebrated his graduation from college by joining a mountain climbing expedition in the French Alps. Dan is in excellent physical condition: he runs 3 to 5 miles daily, and he played intramural soccer, volleyball, and rugby throughout college. At the insistence of his parents, Dan underwent a complete medical examination before the climb, which he passed with flying colors. He was off to the Alps! -The climbers were encouraged to breathe from tanks of 100% O2. What is the Po2 of 100% humidified O2 on Mont Blanc? -What percent of supplemental O2 would be required to restore Dan's PaO2 to 100 mm Hg?

Po2 = (Pb - PH2O) x FIO2 = (420 mm Hg - 47 mm Hg) x 1.00 = 373 mm Hg So have to calculate in PACO2/R PAO2= (Pb-47) x 21% - PACO2/R So 100= (420-47) x ? - 40mmHg/.8 100= 373 x ? - 50mmHg 150 = 373 x ? 150/373= ? FiO2 = .40/40% for answer below 40% FIO2

What is Perfusion limited: ?

Pp gradient is not maintained, only way to increase amount of gas is to increase blood flow. Gases that are perfusion limited have their partial pressures equilibrated with the alveolar pressure before exiting the capillary, the Pp of CO (diffusion limited) does not reach equilibrium.

Characteristics of pulmonary arteries and pulmonary capillaires?

Pulmonary arteries have thin and distensible walls with low smooth muscular tone so they are highly compliant. Once the blood leaves the pulmonary arteries they will enter the arterioles and then into the capillaries which have a very low vascular resistance to flow and a high capacity for volume b/c under normal conditions the number of capillaries that are open and available to receive blood is relatively low. Under periods of stress or exercise the number of capillaries that can be recruited to receive this blood flow goes up drastically. So as you recruit more capillaries to receive this increased blood flow this allows the pulmonary vasculature to keep this resistance(PVR) low.

Expiratory center is responsible for expiration(Duh!) and is really only active when?

Really only active in exercise; under normal conditions the expiratory center will not be active since expiration is a passive process.

Sinusitis aka?

Rhinosinusitis

Laryngitis viral Etiopathogenesis?

Rhinovirus, parainfluenza virus, RSV, coronavirus, adenovirus, influenza

How can you measure pulmonary blood pressure?

Right heart catheterization (this is gold-standard to determine if someone has pulmonary arterial HTN)

What is The main causes of drowning at swimming pools?

Shallow Water Blackout; Connected with the dangerous practice of hyperventilation coupled with underwater breath holding

So the bottom line here is that when you are awake you are most responsive to increases in PaCO2. Notice that when you sleep ventilatory drive decreases. So your body pH decreases when sleeping (this is important since there are some disorders that are pH sensitive ex include: sickle cell anemia, paroxysmal nocturnal hematuria and more). Furthermore, when you take barbiturates etc in high enough quantities you can forget to breathe. metabolic acidosis is where we are most sensitive to changes in PaCO2 when we sleep our respiratory rate goes down and it requires a greater PaCO2 to get us to ventilate. morphine, barbiturates, COPD: we are less likely to ventilate when we are exposed to one of these things. When you are awake you are most responsive to changes/increases in PaCO2

So the bottom line here is that when you are awake you are most responsive to increases in PaCO2. Notice that when you sleep ventilatory drive decreases. So your body pH decreases when sleeping (this is important since there are some disorders that are pH sensitive ex include: sickle cell anemia, paroxysmal nocturnal hematuria and more). Furthermore, when you take barbiturates etc in high enough quantities you can forget to breathe. metabolic acidosis is where we are most sensitive to changes in PaCO2 when we sleep our respiratory rate goes down and it requires a greater PaCO2 to get us to ventilate. morphine, barbiturates, COPD: we are less likely to ventilate when we are exposed to one of these things. When you are awake you are most responsive to changes/increases in PaCO2

Boyle Law?

The relationship between the pressure and volume of a gas at constant temperture; when volume increase, pressure decreases. ↑ in external pressure → decrease in gas volume and vice versa Another definition: The volume of gas will change depending on the outside pressure (actual volume) Gases are compressible

Peripheral Chemoreceptors are most sensitive to what molecule?

These are MOST sensitive to O2(but is also responsive to CO2 and H+ just not as much) BUT they don't respond to O2 until it is below 60 mmHg (normal is 60-100 mm Hg).

What happens in the first few days when you go to high altitude?

They breathe excessively(hyperventilation) and burn extra energy even when the body is relaxed. The heart rate then gradually decreases as you acclimatize.

What do the irritant receptors of the lungs do?

They go via vagus nerve to the medulla and they cause constriction. Irritant receptors, really cause you to stop breathing. Remember back in HS chemistry, when the teacher told you not to inhale that HCl, but to use 2 fingers to fan the fumes to your nose. And what do you do, what did I do, what did everyone do? Yup, put our nose over it and tried to take a deep breath. So not only did this damage our lungs the irritant receptors became activated.

Bronchial arteries carry blood where?

They originate at the aorta, and carries blood to non-alveolar regions of the lungs - including connective tissue, septa, and bronchi - providing nourishment to these areas. Blood in the bronchial circulation is returned to the left atrium, and therefore is not oxygenated.

What is the A-a Gradient used for?

To compare the causes of hypoxemia and the existence of a shunt or not.

what determines lung capillary beds contributions to the vascular resistance?

Unlike capillary beds in other organs, alveolar capillary beds contribute significantly to the resistance of the pulmonary circulation (about 40%), and its contribution varies depending on the lung volume. As the lung expands/increase, stretch of the alveolar wall compresses the alveolar capillaries and elevates PVR. At the same time, the extra-alveolar vessels are pulled open due to recoil forces. The opposite is true at low lung volumes. The net result is that perfusion of the pulmonary vasculature is optimal at or near FRC.

What will the V/Q ratio equal with a physiological shunt?

V/Q=0 The lung without ventilation has a V/Q of 0. Because there is not gas exchange to blood leaving the unit continues to be mixed venous blood. This condition can be known as atelectasis (obstruction to ventilation of a gas exchanging unit with subsequent loss of volume).

Where is the Expiratory center?

Ventral respiratory group of medulla

How can viagra be used for mountain climbers?

Viagra(sildenafil) protects mountain climbers' lungs from problems associated with high altitude, such as pulmonary hypertension, researchers say. Pulmonary hypertension can be triggered by a lack of oxygen. According to research carried out at the University of Geissen, Germany, Viagra protects the lungs of mountain climbers from pulmonary hypertension. You can read about this study in the journal Annals of Internal Medicine. The scientists say this discovery could give Viagra another indication - not just for mountain climbers, but patients who develop pulmonary hypertension (without climbing mountains). If you have pulmonary hypertension your heart has to work a lot harder as the blood vessels around your lungs constrict. You can suffer heart damage, heart attacks and even death. The researchers got a group of 14 healthy male volunteer mountain climbers to see whether Viagra would offer them any benefits with regards to pulmonary hypertension. Half the group were given Viagra while the other half got a placebo (dummy drug). The group was tested at sea level and then again when they were at the Mount Everest Base Camp. It seems that the Viagra reduced their blood pressure as well as enhancing the transport of oxygen to their lungs - both at sea level and high altitude. This is the first time any drug has been shown to enhance exercise capacity at both sea level and high altitude. The researchers said the penis and the lungs both share a biochemical similarity. Both the penis and the lungs have lots of phosphodiesterase, this is an enzyme which constricts blood vessels in the lungs. Viagra (sildenafil) stops the enzyme from working, the result being better erections and blood supply to the walls of the lungs.

Tonsillitis viral Etiopathogenesis?

Viral: rhinovirus, RSV, adenovirus, coronavirus

What is Ventilation?

Volume of Air Delivered or Flowing Through a Compartment

What is Alveolar Ventilation?

Volume of air entering or leaving the alveoli per minute

Difference in blood flow in the lungs when supine compared to when standing?

When supine blood flow though lung is uniform in the lungs. When you stand, blood flow is unequal (mainly due to gravity). Blood pools lower than the heart

How to get pulmonary venous pressure and left atrial pressure?

When the catheter is wedged, a mean pressure of ~6 mm Hg is recorded. Assuming a standing column of blood exists distal to the end of the catheter, this pressure represents pulmonary venous pressure. pulmonary wedge pressure(mean of 6mm Hg) will represent the pulmonary venous pressure and the left atrial pressure.

Effect of Shunts on PaO2 chart with tons of info:

X-axis: we are increase the inspired pP of the O2. Y-axis: increasing pPO2 in the arterial blood. with no shunt we essentially have a linear relationship/increase in the amount of arterial O2 as it relates to thepP of inspired O2. So with no shunt as you increase the inspired PO2 you will have a 1:1 increase in arterial PO2 with a physiological shunt you can increase an arterial O2 by giving 100% O2(which corrects the V/Q mismatch) BUT with an anatomical shunt you cannot increase the arterial O2 when giving 100% O2 b/c you still have a significant amount of blood that is bypassing the lungs completely. In the absence of a shunt, PIO2 has a direct effect on PaO2. With an increase in shunting, the effect of PIO2 on PaO2 is reduced. Note that the amount of O2 in the soluble form is far less than the amount than can be carried on Hb. At low shunt fractions, the amount of O2 dissolved in the blood exiting the ventilated alveoli is sufficient to load the Hb in the blood exiting poorly ventilated alveoli. As an increasing fraction of the blood is shunted away from ventilated alveoli, there is an exponentially increasing number of O2 binding sites on Hb and a decreasing amount of dissolved O2 to fill them. With a 50% shunt, there is almost no increase of PaO2 with increased PIO2 above atmospheric levels. In a physiological shunt, blood perfuses alveoli that are poor ventilated and have a low PaO2. The blood from these lung units have a low oxygen content, and when this blood mixes with oxygen from lung units with normal V/Q ratios, the PaO2 is decreased, and AaDO2 increases. A key feature in diagnosing an anatomical shunt is to verify a higher than normal AaDO2 and then determine the effect of inspiring pure O2 on the AaDO2. In the case of an anatomical shunt, inspiring 100% O2 does not bring PaO2 back to normal. Under normal conditions, hemoglobin in blood passing through the lungs is maximally oxygenated. Therefore, the only increase in O2 that can result is from replacing N2 in the blood perfusing the alveolar capillaries. Since the shunted blood never enters the alveolar capillaries, O2 cannot replace the N2, and a large AaDO2 will continue to exist. PaCO2 is not affected by the anatomic shunt. This is because of two factors. First, the blood CO2 level is tightly regulated. So, as PaCO2 starts to rise, respiration rate is increased, which increases CO2 elimination from the blood perfusing the alveolar capillaries and lowers the PCO2 level in the pulmonary vein blood. Mixing the pulmonary vein blood with a low PCO2 with the shunt blood that has a high PCO2 yields a normal PaCO2. with the shunt blood, PaCO2 2nd, O2 comes into equilibrium with the blood very rapidly in the alveolar capillaries. In addition, CO2 continues to diffuse across the alveolar capillaries as long as the blood is traversing these vessels. Thus, as alveolar ventilation increases, CO2 is removed from the alveoli, and CO2 can continue to diffuse out of the blood. If a patient with a physiological shunt breaths 100% O2, even poorly ventilated alveoli will receive O2, increasing PAO2 in these alveoli. In addition, over a 15 minute period, the N2 in the blood and poorly ventilated alveoli will be replaced with O2. Thus, the PaO2 will be elevated considerably in these patients. In contrast, with an anatomical shunt, a part of the blood is continually shunted around the lungs, so the N2 level remains elevated, and PaO2 cannot be restored. In some cases, anatomical and physiological shunts are distinct entities; but, there are times when it is better if you think of them as part of a continuum of V/Q mismatch. An anatomical shunt is where V/Q = 0. For example, there is no ventilation of the bronchial circulation, but it is perfused; so the V/Q is 0, and blood passing through the bronchial circulation lowers the PaO2, and inspiring 100% O2 does not correct the AaDO2. Physiological shunts are regions of the lung where V/Q is low, but not 0. A low V/Q will increase venous admixture and lower PaO2, but if the region has at least partial ventilation, then 100% O2 should correct the AaDO2. Consider pneumonia. As pneumonia progresses, ventilation will progressively decrease. At some point, the ventilation to different regions of the lungs will be reduced to the point where O2 is not transferred to the blood perfusing those regions, even if the subject is breathing 100% O2. At that point, the physiological shunt has converted to a true shunt, or anatomical shunt.

Which Zone has a pCO2 closest to that of mixed venous blood?

Zone 3

How does right heart catheterization work to figure out the pulmonary blood pressures?

a balloon-tipped catheter is advanced into a peripheral vein. Inflation of the balloon causes the catheter tip to be carried by the blood into the right ventricle. As the tip advances further, the blood pressure in the pulmonary artery can be measured. Eventually, the tip will wedge the artery, cutting off the circulation. Distal to the end of the wedged catheter, the blood vessels contain blood. So, a static pressure is recorded that equals the pulmonary vein and left atrial pressure.

how to determine normal A-a gradient with age?

age + 10 divided by 4 = what you A-d gradient should be for your age. So for me its 30 + 10 = 40 and 40/4 = 10 mmHg

Alveolar capillaries vessel diameter is affected by?

alveolar pressure & stretch of the alveolar wall

which pressures dominate in zone 1 of the lungs?

alveolar pressure >arterial pressure >venous pressure

V/Q ratio in zone 1?

blood flow is alot lower while ventilation is lower but not as much as blood flow is so the V/Q is elevated

What is mostly the cause of an increase in vascular resistance in the lungs?

capillary vessels have fairly low vascular resistance. the increase in vascular resistance is largely due to the extra-alveolar vessels.

Which Peripheral Chemoreceptors are the only ones that respond to changes in pH (H+)?

carotid bodies ONLY

High altitude sickness is compounded by related symotoms such as ?

cerebral edema(HACE) (swelling of brain) and pulmonary edema (fluid accumulation in lungs).

when is O2 diffusion limited?

fibrosis and exercise fibrosis hinder diffusion by making barrier to diffusion thicker(fibrotic) Exercise can make O2 diffusion limited b/c when you exercise your CO increase which is bringing more blood to the lungs and thus the lungs recruit more capillary beds and now that is greatly increase surface area and perfusion so there is plenty of blood getting there now so its up to if your lungs can match it; how quickly can I get O2 to diffuse into what available

Lung stretch receptors are located where?

in smooth muscle cells within the lung

What happens to the A-a gradient with an Anatomic shunt?

increased

Sleep Apnea ?

increased frequency and duration of apnea during sleep

Laryngitis most common Etiopathogenesis?

infectious

Definition of Rhinosinusitis?

inflammation of nasal cavity and paranasal sinuses

Definition of Rhinitis?

inflammation of nasal mucosa

Definition of Pharyngitis?

inflammation of oropharyngeal mucosa

Definition of Tonsillitis?

inflammation of the tonsils

Perfusion (Q) equation?

refers to pulmonary blood flow (HR X RV stroke volume)

Regional differences in V/Q and PCO2/PO2: as we move up the lung we are having an increase in ?

ventilation relative to perfusion. (really ventilation and perfusion both decrease as we move up the lung but perfusion just decreases at a much higher rate than does ventilation so relative to one another ventilation will be higher than blood perfusion as you move up the lung.

Allergic Rhinitis Epidemiology?

•10-30% of adults and children •Most patients develop symptoms as children or young adults

Cheyne-Stokes Respiration: -Describe its character pattern

•Abnormal pattern of breathing characterized by progressively deeper and sometimes faster breathing, followed by a gradual decrease that results in a temporary stop in breathing called an apnea. •The pattern repeats, with each cycle usually taking 30 seconds to 2 minutes. •Oscillation of ventilation between apnea and hyperpnea with a crescendo-diminuendo pattern.

The Common Cold (Rhinosinusitis): -Acute length? -Chronic length?

•Acute: < 4 weeks; most commonly viral •Chronic: > 12 weeks most common causes of Rhinosinusitis is viral but if it lasts longer than 4 weeks you may need to look into it being caused by something else.

Croup (laryngotracheitis) bacterial Etiopathogenesis?

•Bacterial (S. aureus, S. pneumoniae, S. pyogenes, alpha hemolytic strep spp., Moraxella catarrhalis) •Thick pus in subglottic trachea; ulcerations, pseudomembranes, microabscesses of mucosa

What happens with The Bends?

•Caused by the formation of bubbles of gas that occur with changes in pressure during scuba diving. As the pressure due to nitrogen increases, more nitrogen dissolves into the tissues. •The longer a diver remains at depth, the more nitrogen dissolves. •Unlike the oxygen in the air tank a diver uses to swim underwater, the nitrogen gas is not utilized by the body and builds up over time in body tissues. As a diver swims to the surface, the pressure due to nitrogen decreases. The nitrogen, which has dissolved in tissues, wants again to leave, because the body can hold only a certain amount based on that nitrogen pressure.

Pharyngitis lab tests?

•Centor criteria score ≥3, test for GAS •Guidelines vary; use clinical judgment •Rapid antigen detection test •Culture for high-risk groups

Nonallergic rhinitis?

•Chronic presence of nasal congestion, rhinorrhea, or postnasal drainage •Diagnosis of exclusion •Symptoms are perennial(last all year which is different from allergic rhinitis)

What is Henry's Law?

•Concentration of gas dissolved (Cx) = Px partial pressure of the gas X solubility of the gas •Cx = Px X solubility (for oxygen, it is a constant 0.003 mm Hg) •So if partial pressure of oxygen is 100 mmHg, Henry's law converts the partial pressure of gas to concentration of gas in liquid phase (e.g. blood) •The concentration of a gas in solution is expressed as volume percent (%) or mL gas/100 ml blood

Inspiratory Center: -What does it do? -Receives input from where? -Sends output how and where? -Affected by what 2 centers?

•Controls basic rhythm by setting frequency •Receives input form glossopharyngeal and vagus (IX and X) •Sends output by phrenic nerve to diaphragm •Affected by Pneumotactic and Apneustic centers in pons

Fick's Law (Diffusion of Gas)?

•Diffusion is directly proportional to the driving force, diffusion coefficient, and the surface area. It is inversely proportional to the thickness of the membrane. •Driving force (partial pressure differences of the gases) •Diffusion coefficient - depends on molecular weight and solubility •Thickness of membrane; more mucus means longer distance to travel. •V = flow •A = surface area for exchange •increase in exercise •decrease in emphysema •T = thickness of the membrane •Increases in fibrosis •D = diffusion constant •P1 - P2 = partial pressure gradient Surface area of the lungs can increase or decrease, we can recruit more of the lungs with greater blood flow (cardiac output) we breathe deeper. In emphysema, the surface of the lungs is increased but the "springyness (aka they become too compliant)" of the lungs is compromised so we do not generate the proper pressure gradients for gases to flow. Also, we destroy some of the cells (type 1 pneumocytes) that allow diffusion.

Tonsillitis Pathogenesis?

•Either bacterial or viral infection of tonsils •Some pathogens may cause irritation secondary to nasal secretions •Excess secretion and edema and inflammatory cytokine production cause symptoms

Diffusing capacity of CO, O2, and CO2

•Graph shows the diffusing capacities of O2, CO2 and CO. •CO2 really diffuses easily

Pharyngitis bacterial Etiopathogenesis?

•Group A streptococcus (5-15% of cases) •Less common causes: Group C and G strep, Mycoplasma pneumoniae, Chlamydia pneumoniae, Arcanobacterium haemolyticum, C. diphtheriae, Francisella tularensis, STIs

Lungs - Hypoxic Vasoconstriction?

•If oxygen for some reason is decreased to certain parts of the lungs, then blood flow is reduced known as - hypoxic vasoconstriction - (the lungs only want to have blood flow where it can get adequate O2 supplied.) •This is opposite from other organs where hypoxia causes vasodilatation •This is important to divert blood from poorly ventilated to well ventilated areas. •But what if all areas of the lungs have decreased O2 content (e.g. climbing a mountain) Fetal pulmonary vascular resistance is very high because of generalized hypoxic vasoconstriction. As a result, blood flow thought the fetal lungs is low. With the first breath, the alveoli of the neonate are oxygenated, and pulmonary vascular resistance decreases, and pulmonary blood flow increases and becomes equal to cardiac output.

Sinusitis: •Epidemiology?

•Incidence higher in women •Highest incidence in patients 45-64 years old •Risk factors: ↑ age, smoking, air travel, swimming, asthma/allergies, immunodeficiency, dental disease

Laryngitis pathogenesis for infection?

•Inflammation and congestion lead to an immune response •WBC arrive to clear out pathogens •Edema of vocal cords and surrounding tissue changes vibrations and fluid-wave dynamics •Chronic irritation or inflammation can lead to Reinke's edema (polypoid corditis) •Due to smoking, laryngopharyngeal reflux/GERD, hypothyroidism

What is the main thing that messes with PVR?

•Low PAO2 and high PACO2 causes vasoconstriction (this is different from the rest of circulation), which decreases blood flow to poorly ventilated regions of the lung. In contrast, high PAO2 increases perfusion of a region.Lungs undergo hypoxic vasoconstriction! The idea is that poorly ventilated areas of lungs will get less blood flow while better ventilated areas get more blood

Laryngitis Epidemiology?

•More common in adults (18-40) •Typically lasts 3-7 days

Peripheral Chemoreceptors all actions:

•O2 but below 60 mm Hg (normal is 60-100 mm Hg). •Increase in arterial PCO2; should be kept at 40 mm Hg (for a pH of 7.4) •Decrease in pH (H+ receptors only in carotid bodies)

What sensory input does the inspiratory center receive?

•Peripheral Chemoreceptors -> Glossopharyngeal and Vagus nerves ->Inspiratory center and •Lung stretch (Mechanoreceptors) -> Vagus nerve -> Inspiratory center

What does the Apneustic center stimulation (Lower Pons) do?

•Prolongs inspiration -> Brief expiratory movement •Due to a Prolongation of action potential duration in phrenic nerve •Prolongs the contraction of diaphragm

Pharyngitis viral Etiopathogenesis?

•Respiratory viruses (25-45% of cases): Adenovirus, rhinovirus, coronaviruses, enteroviruses, influenza, parainfluenza, RSV •EBV, herpes simplex virus, CMV, HIV

Allergic Rhinitis presentation?

•Rhinorrhea, nasal congestion, sneezing, nasal itching (particularly kids), allergic conjunctivitis, poor sleep, fatigue, snoring, headaches •PE: allergic shiners, transverse nasal crease (kids), edematous and pale nasal mucosa

relationship b/w CO2 production, PACO2 and ventilation?

•So if CO2 production is constant then PACO2 is determined by alveolar ventilation •Conversely, if ventilation is held constant but CO2 production is increased then PACO2 increases Alveolar ventilation is proportional to CO2 production Alveolar ventilation is inversely proportional to PACO2 In the steady state, CO2 production must be balanced by CO2 elimination. Therefore, alveolar ventilation must be proportional to CO2 production. Therefore, in the normal subject, metabolism and ventilation (breathing frequency and tidal volume) will be matched, and imbalance in these parameters will quickly lead to CO2 and pH imbalance.

Tonsillitis presentation?

•Sore throat, fever, tonsillar exudates, tender cervical lymphadenopathy •Very similar to pharyngitis •Chronic tonsillitis lasts ≥ 3 months

Symptoms and Tx of PE?

•Symptoms may include 1.difficulty breathing 2.pain in the chest during breathing 3.in more severe cases collapse, circulator instability and sudden death. Treatment anticoagulant medication, such as heparin and warfarin, and rarely (in severe cases) with thrombolysis or surgery.

What will occur with ventilation with a R-L shunt?

•Ventilation is increased (due to increased CO2-central chemoreceptor) but some (shunted) blood will still be un-oxygenated. Central chemoreceptors will sense an increase in CO2 and increase ventilation and reduce arterial PCO2 to keep it in the normal range.

Croup (laryngotracheitis) viral Etiopathogenesis?

•Viral (parafluenza, influenza, RSV, rhinovirus, measles, enterovirus) •Virus infects mucosal epithelia and spreads locally; inflammation causes narrowing of subglottic airway

Pathophysiology of The Common Cold (Rhinosinusitis)?

•Viral infection causes inflammation, can impair mucociliary clearance •Hypersecretion and ↑ vascular permeability lead to fluid in nasal cavity/sinuses •Secondary bacterial infection occurs in small percentage of patients

Pharyngitis Presentation?

•Viral: URTI symptoms, rash •Bacterial: acute onset pharyngitis, fever, pharyngeal edema, tender cervical lymphadenopathy

Laryngitis presentation?

•Voice changes, vocal fatigue, throat pain/dryness, dry cough •Acute resolves within 2 weeks •Chronic lasts more than 3 weeks •Vocal strain may damage vocal cords